Esther Redin, Harsha Sridhar, Yingqian A. Zhan, Barbara Pereira Mello, Hong Zhong, Vidushi Durani, Amin Sabet, Parvathy Manoj, Irina Linkov, Juan Qiu, Richard P. Koche, Elisa de Stanchina, Maider Astorkia, Doron Betel, Álvaro Quintanal-Villalonga, Charles M. Rudin
{"title":"更正:SMARCA4通过调控神经内分泌转录因子和REST剪接控制小细胞肺癌的状态可塑性","authors":"Esther Redin, Harsha Sridhar, Yingqian A. Zhan, Barbara Pereira Mello, Hong Zhong, Vidushi Durani, Amin Sabet, Parvathy Manoj, Irina Linkov, Juan Qiu, Richard P. Koche, Elisa de Stanchina, Maider Astorkia, Doron Betel, Álvaro Quintanal-Villalonga, Charles M. Rudin","doi":"10.1186/s13045-024-01609-7","DOIUrl":null,"url":null,"abstract":"<p><b>Correction: Journal of Hematology & Oncology (2024) 17:58 </b><b>https://doi.org/10.1186/s13045-024-01572-3</b></p><br/><p>The original article mistakenly omitted numerous elements from the article figures due to an error in transferring the files at the proofing stage. The figures have since been updated to restore all missing elements of each affected figure (Figs. 1, 2, 3, 4, 5, 6).</p><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 1</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig1_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 1\" aria-describedby=\"Fig1\" height=\"717\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig1_HTML.png\" width=\"685\"/></picture><p><i>SMARCA4</i> expression correlates with NE features in SCLC.<b> A</b> <i>SMARCA4</i> mRNA levels in cell lines derived from 30 tumor types assessed using the Cancer Cell Line Encyclopedia (CCLE). Bars indicate the median expression per tumor type. <b>B</b> <i>SMARCA4</i> mRNA levels in LUAD and SCLC specimens retrieved from Quintanal Villalonga et al. [27]. Student’s two-tailed unpaired t test. **<i>p</i> < 0.01. <b>C</b> Spearman correlation of <i>SYP, CHGA, INSM1, YAP1</i> and <i>REST</i> with <i>SMARCA4</i> mRNA levels in Rudin et al. and George et al. databases and CCLE[25, 26]. <b>D</b> <i>SMARCA4</i> mRNA expression in low and high NE SCLC tumors in cell lines (CCLE) and clinical specimens (Rudin et al. and George et al.) [25, 26]. One-way ANOVA test followed by Bonferroni post-hoc test. ****<i>p</i> < 0.0001, ***<i>p</i> < 0.001, **<i>p</i> < 0.01. <b>E</b> Western blotting of ASCL1, NEUROD1, SYP and CHGA in isogenic cell lines derived from H82 and H146 expressing different combinations of shRNAs against <i>SMARCA4</i> and/or <i>SMARCA2</i>. Expression of shRNAs from <b>E</b> was conditional of doxycycline treatment. Protein collection and blotting was performed after 14 days of doxycycline treatment. See also Fig. S1</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 2</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig2_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 2\" aria-describedby=\"Fig2\" height=\"995\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig2_HTML.png\" width=\"685\"/></picture><p>SMARCA4 inhibition suppresses the NE phenotype in SCLC. <b>A</b> Hockey-stick plots of DEGs in FHD-286-treated cells after 14 days (100 nM) versus control, untreated cells. (See Table S1). <b>B</b> Dot plots showing negative enrichment in selected neuronal and NE pathways analyzed by GSEA in RNAseq data from H82 and H146 cell lines treated with FHD-286 versus untreated. (See Table S1). <b>C</b> GSEA applying Zhang et al. NE gene signature [28] in H82 cell line treated with FHD-286 versus untreated. <b>D</b> Heatmaps showing the most significant confident targets (top 25 with TPMs > 2) of NEUROD1 (left) and ASCL1 (right) [7], in H82 (left) and H146 (right) bulk RNAseq (FHD-286 treated vs untreated). <b>E</b> Log<sub>2</sub> fold change of Hippo pathway genes from data in A. Student’s two-tailed unpaired t test. ***<i>p</i> < 0.001, **<i>p</i> < 0.01. The mean ± SD is shown. <b>F</b> Log<sub>2</sub> fold change of NOTCH pathway genes from data in <b>A</b>. Student’s two-tailed unpaired t test. ***<i>p</i> < 0.001, *<i>p</i> < 0.05. The mean ± SD is shown. <b>G</b> Western blotting of H524 (SCLC-N), H82 (SCLC-N), HCC33 (SCLC-N), H69 (SCLC-A), SHP77 (SCLC-A) and H146 (SCLC-A) cells after treatment with 100 nM of FHD-286 for 7 and 14 days.<b> H</b> t-SNE of Zhang NE signature and <i>SMARCA4</i> levels applied to public scRNAseq data of 4 myc-driven murine (RPM) tumors [6]. <b>I</b> Scoring for Zhang NE signature and <i>SMARCA4</i> projected in a pseudotime trajectory from early to late time points in a tumor from a Myc-driven murine SCLC model showing subtype plasticity [6]. See also Figs. S2, S3 and Table S1</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 3</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig3_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 3\" aria-describedby=\"Fig3\" height=\"768\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig3_HTML.png\" width=\"685\"/></picture><p>SMARCA4 inactivation alters chromatin accessibility in NE-high SCLC.<b> A</b> Heatmap showing ATACseq chromatin accessibility changes (FDR:0.01, FC > 1.5) in H82 and H146 cells after treatment with FHD-286 (100 nM, 14 days). <b>B</b> Enrichment of neuronal and NE HOMER transcription factor-binding DNA motifs in ATAC-seq peaks lost after treatment with FHD-286 (100 nM, 14 days). The percentage indicates the amount of target sequences with motif. <b>C</b> Genomic localization of lost and gained accessible sites upon FHD-286 treatment in H82 and H146 cells. <b>D</b> ATACseq genome tracks of <i>NEUROD1</i>, <i>SYP</i> and <i>CHGA</i> in H82 and H146 cells after treatment with FHD-286. Peaks with a significant reduction in chromatin accessibility are indicated with arrows. <b>E</b> Enrich analysis applied to all genes with lost sites (across all gene body) following FHD-286 treatment. Top 10 GO Biological processes enriched are shown. See also Fig. S4</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 4</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig4_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 4\" aria-describedby=\"Fig4\" height=\"841\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig4_HTML.png\" width=\"685\"/></picture><p>SMARCA4 binds to neuronal and NE lineage TF genes in SCLC.<b> A</b> Heatmap and metaplot showing<i>SMARCA4</i> binding profile determined by ChIP-seq in 4 NE SCLC PDXs and a pooled input. The range under the map indicates the ChIP-seq signal intensity. <b>B</b> Metaplots of <i>ASCL1</i> and <i>NEUROD1</i> in all PDXs and input. Heatmaps showing the binding of SMARCA4 to ASCL1 and NEUROD1 gene bodies. The range indicates the normalized enrichment along the respective gene regions. <b>C</b> NE lineage TFs and gene promoter proximal regions (within 1 kb of TSS) bound by SMARCA4 in NE SCLC PDXs. <b>D</b> Dot plot of Poly-Enrich analysis applied to SMARCA4 ChIP-seq peaks. Fold enrichment refers to the fold increase in the signal for a particular gene relative to the background signal. The counts refer to the number of genes detected in the ChIP-seq data that are part of the indicated pathways. <b>E</b> Enrich analysis of 617 consensus genes selected by combining RNAseq from Fig. 2 and ChIP-seq data. See also Fig. S5E. <b>F</b> Enrichment analysis of TF-binding motifs in the SMARCA4 ChIP-seq data identified with HOMER. See also Figs. S5, S6 and Table S3</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 5</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig5_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 5\" aria-describedby=\"Fig5\" height=\"876\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig5_HTML.png\" width=\"685\"/></picture><p>SMARCA4 regulates SRRM4 expression to control splicing and activation of REST. <b>A</b> Venn diagram of ASCL1 and NEUROD1 published binding targets from Borromeo et al. [7] overlapping with genes downregulated by FHD-286 in H146 and H82 cells. <b>B</b> Western blots of H82 and H146 cells treated with FHD-286 for 14 days. <b>C</b> Metaplot of SMARCA4 ChIP-seq showing SMARCA4 binding to <i>SRRM4</i> in 4 NE SCLC PDXs. Range indicates the fold enrichment with respect the input. ChIP-seq genome tracks at SRRM4 TSS. Graphs were obtained from IGV. <b>D</b> Correlation of <i>SMARCA4</i> and <i>SRRM4</i> mRNA levels in SCLC patients’ database. Spearman correlation. <b>E</b> Correlation analysis of <i>SRRM4</i> and <i>SMARCA4</i> in cancer cell lines retrieved from CCLE. Cell lines with both high <i>SMARCA4</i> and <i>SRRM4</i> mRNA levels are highlighted. <b>F</b> Merged ATAC-seq tracks of H82 and H146 parentals cells and FHD-286 treated cells (day 14) at SRRM4 gene locus visualized with IGV. <b>G</b> Graphical representation of REST genomic regions and spliced isoforms with the binding location of the different primers used for PCR. <b>H</b> PCR analysis of <i>REST</i> splicing isoforms using two pairs of primers (E2F1 + E4R1 and E1F1 + E4R1) that span N3c. <b>I</b> RT-qPCR of REST4 isoforms (S3, S7, S12) in H82, H146 and H524 treated with FHD-286 (14 days) versus untreated cells. The pair of primers E3N3c and E4R2 that recognizes all isoforms including exon N3c was used. Student’s two-tailed unpaired t test. ***<i>p</i> < 0.001. The mean ± SD is shown. <b>J</b> Enrich analysis applied to commonly and significantly downregulated genes in both H146 and H82 (n = 904) cell lines identified in the bulk-RNAseq (Fig. 2). See also Fig. S7</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 6</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig6_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 6\" aria-describedby=\"Fig6\" height=\"989\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig6_HTML.png\" width=\"685\"/></picture><p>SMARCA4/2 inhibition by FHD-286 induces ERBB signaling and sensitivity to afatinib in SCLC. <b>A</b> Proliferation curves of SCLC-A, -N, -P and -Y SCLC cell lines treated with FHD-286 for 96 h. The mean ± SD is shown. <b>B</b> Tumor growth of Lx151 and Lx95 SCLC PDXs implanted in NSG mice and treated with 1.5 mg/kg BID p.o. of FHD-286. Student’s two-tailed unpaired t test. ***<i>p</i> < 0.001. <b>C</b> IPA analysis on significantly upregulated genes in FHD-286-treated cells versus control untreated cells. <b>D</b> Immunoblot of ERBB family proteins in H146 and H82 cells after treatment with 100 nM of FHD-286 for 14 days. <b>E</b> Western blots of FHD-286 (100 nM) treated cells at the indicated times. <b>F</b> Synergy plots of FHD-286 and afatinib in NE SCLC cell lines. <b>G</b> Cell death quantification by flow cytometry at day 5 of H146 and H82 cells after treatment with FHD-286, afatinib or both. One way ANOVA followed by Bonferroni comparison test. ***<i>p</i> < 0.001, ****<i>p</i> < 0.0001. <b>H</b> Normalized tumor growth of Lx1042 (SCLC-N), Lx1322 (SCLC-P), Lx151 (SCLC-A) and Lx95 (SCLC-A) relative to day 1 of treatment. Two-way ANOVA followed by Bonferroni comparison test. *<i>p</i> < 0.05, **<i>p</i> < 0.01, ***<i>p</i> < 0.001. <b>I</b> Schematic representation of the role of SMARCA4 in sustaining the NE phenotype in SCLC</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><h3>Authors and Affiliations</h3><ol><li><p>Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA</p><p>Esther Redin, Harsha Sridhar, Barbara Pereira Mello, Hong Zhong, Vidushi Durani, Amin Sabet, Parvathy Manoj, Álvaro Quintanal-Villalonga & Charles M. Rudin</p></li><li><p>Center for Epigenetics Research, Memorial Sloan Kettering Cancer Center, New York, NY, USA</p><p>Yingqian A. Zhan & Richard P. Koche</p></li><li><p>Precision Pathology Center, Memorial Sloan Kettering Cancer Center, New York, NY, USA</p><p>Irina Linkov</p></li><li><p>Antitumor Assessment Core, Memorial Sloan Kettering Cancer Center, New York, NY, USA</p><p>Juan Qiu & Elisa de Stanchina</p></li><li><p>Weill Cornell Medicine Graduate School of Medical Sciences, New York, NY, USA</p><p>Vidushi Durani & Charles M. Rudin</p></li><li><p>Applied Bioinformatics Core, Weill Cornell Medicine, New York, NY, 10065, USA</p><p>Maider Astorkia & Doron Betel</p></li><li><p>Division of Hematology and Oncology, Department of Medicine, Weill Cornell Medicine, New York, NY, 10065, USA</p><p>Doron Betel</p></li><li><p>Department of Physiology, Biophysics and Systems Biology, Institute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, 10065, USA</p><p>Doron Betel</p></li></ol><span>Authors</span><ol><li><span>Esther Redin</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Harsha Sridhar</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Yingqian A. Zhan</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Barbara Pereira Mello</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Hong Zhong</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Vidushi Durani</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Amin Sabet</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Parvathy Manoj</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Irina Linkov</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Juan Qiu</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Richard P. Koche</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Elisa de Stanchina</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Maider Astorkia</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Doron Betel</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Álvaro Quintanal-Villalonga</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Charles M. Rudin</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li></ol><h3>Corresponding authors</h3><p>Correspondence to Álvaro Quintanal-Villalonga or Charles M. Rudin.</p><h3>Publisher's Note</h3><p>Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.</p><h3>Lead Contact: </h3><p> Charles M. Rudin</p><h3>Additional file 1.</h3><p><b>Open Access</b> This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. 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0-.92-.08-1.33-.25-.41-.16-.77-.4-1.08-.7-.3-.31-.54-.69-.72-1.13-.17-.44-.26-.95-.26-1.52zm4.61-.62c0-.55-.11-.98-.34-1.28-.23-.31-.58-.47-1.06-.47-.41 0-.77.15-1.08.45-.31.29-.5.73-.57 1.3zm3.01 2.23c.31.24.61.43.92.57.3.13.63.2.98.2.38 0 .65-.08.83-.23s.27-.35.27-.6c0-.14-.05-.26-.13-.37-.08-.1-.2-.2-.34-.28-.14-.09-.29-.16-.47-.23l-.53-.22c-.23-.09-.46-.18-.69-.3-.23-.11-.44-.24-.62-.4s-.33-.35-.45-.55c-.12-.21-.18-.46-.18-.75 0-.61.23-1.1.68-1.49.44-.38 1.06-.57 1.83-.57.48 0 .91.08 1.29.25s.71.36.99.57l-.74.98c-.24-.17-.49-.32-.73-.42-.25-.11-.51-.16-.78-.16-.35 0-.6.07-.76.21-.17.15-.25.33-.25.54 0 .14.04.26.12.36s.18.18.31.26c.14.07.29.14.46.21l.54.19c.23.09.47.18.7.29s.44.24.64.4c.19.16.34.35.46.58.11.23.17.5.17.82 0 .3-.06.58-.17.83-.12.26-.29.48-.51.68-.23.19-.51.34-.84.45-.34.11-.72.17-1.15.17-.48 0-.95-.09-1.41-.27-.46-.19-.86-.41-1.2-.68z" fill="#535353"/></g></svg>\" width=\"57\"/><h3>Cite this article</h3><p>Redin, E., Sridhar, H., Zhan, Y.A. <i>et al.</i> Correction: SMARCA4 controls state plasticity in small cell lung cancer through regulation of neuroendocrine transcription factors and REST splicing. <i>J Hematol Oncol</i> <b>17</b>, 89 (2024). https://doi.org/10.1186/s13045-024-01609-7</p><p>Download citation<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><ul data-test=\"publication-history\"><li><p>Published<span>: </span><span><time datetime=\"2024-09-29\">29 September 2024</time></span></p></li><li><p>DOI</abbr><span>: </span><span>https://doi.org/10.1186/s13045-024-01609-7</span></p></li></ul><h3>Share this article</h3><p>Anyone you share the following link with will be able to read this content:</p><button data-track=\"click\" data-track-action=\"get shareable link\" data-track-external=\"\" data-track-label=\"button\" type=\"button\">Get shareable link</button><p>Sorry, a shareable link is not currently available for this article.</p><p data-track=\"click\" data-track-action=\"select share url\" data-track-label=\"button\"></p><button data-track=\"click\" data-track-action=\"copy share url\" data-track-external=\"\" data-track-label=\"button\" type=\"button\">Copy to clipboard</button><p> Provided by the Springer Nature SharedIt content-sharing initiative </p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"22 1","pages":""},"PeriodicalIF":29.5000,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Correction: SMARCA4 controls state plasticity in small cell lung cancer through regulation of neuroendocrine transcription factors and REST splicing\",\"authors\":\"Esther Redin, Harsha Sridhar, Yingqian A. Zhan, Barbara Pereira Mello, Hong Zhong, Vidushi Durani, Amin Sabet, Parvathy Manoj, Irina Linkov, Juan Qiu, Richard P. Koche, Elisa de Stanchina, Maider Astorkia, Doron Betel, Álvaro Quintanal-Villalonga, Charles M. Rudin\",\"doi\":\"10.1186/s13045-024-01609-7\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><b>Correction: Journal of Hematology & Oncology (2024) 17:58 </b><b>https://doi.org/10.1186/s13045-024-01572-3</b></p><br/><p>The original article mistakenly omitted numerous elements from the article figures due to an error in transferring the files at the proofing stage. The figures have since been updated to restore all missing elements of each affected figure (Figs. 1, 2, 3, 4, 5, 6).</p><figure><figcaption><b data-test=\\\"figure-caption-text\\\">Fig. 1</b></figcaption><picture><source srcset=\\\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig1_HTML.png?as=webp\\\" type=\\\"image/webp\\\"/><img alt=\\\"figure 1\\\" aria-describedby=\\\"Fig1\\\" height=\\\"717\\\" loading=\\\"lazy\\\" src=\\\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig1_HTML.png\\\" width=\\\"685\\\"/></picture><p><i>SMARCA4</i> expression correlates with NE features in SCLC.<b> A</b> <i>SMARCA4</i> mRNA levels in cell lines derived from 30 tumor types assessed using the Cancer Cell Line Encyclopedia (CCLE). Bars indicate the median expression per tumor type. <b>B</b> <i>SMARCA4</i> mRNA levels in LUAD and SCLC specimens retrieved from Quintanal Villalonga et al. [27]. Student’s two-tailed unpaired t test. **<i>p</i> < 0.01. <b>C</b> Spearman correlation of <i>SYP, CHGA, INSM1, YAP1</i> and <i>REST</i> with <i>SMARCA4</i> mRNA levels in Rudin et al. and George et al. databases and CCLE[25, 26]. <b>D</b> <i>SMARCA4</i> mRNA expression in low and high NE SCLC tumors in cell lines (CCLE) and clinical specimens (Rudin et al. and George et al.) [25, 26]. One-way ANOVA test followed by Bonferroni post-hoc test. ****<i>p</i> < 0.0001, ***<i>p</i> < 0.001, **<i>p</i> < 0.01. <b>E</b> Western blotting of ASCL1, NEUROD1, SYP and CHGA in isogenic cell lines derived from H82 and H146 expressing different combinations of shRNAs against <i>SMARCA4</i> and/or <i>SMARCA2</i>. Expression of shRNAs from <b>E</b> was conditional of doxycycline treatment. Protein collection and blotting was performed after 14 days of doxycycline treatment. See also Fig. S1</p><span>Full size image</span><svg aria-hidden=\\\"true\\\" focusable=\\\"false\\\" height=\\\"16\\\" role=\\\"img\\\" width=\\\"16\\\"><use xlink:href=\\\"#icon-eds-i-chevron-right-small\\\" xmlns:xlink=\\\"http://www.w3.org/1999/xlink\\\"></use></svg></figure><figure><figcaption><b data-test=\\\"figure-caption-text\\\">Fig. 2</b></figcaption><picture><source srcset=\\\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig2_HTML.png?as=webp\\\" type=\\\"image/webp\\\"/><img alt=\\\"figure 2\\\" aria-describedby=\\\"Fig2\\\" height=\\\"995\\\" loading=\\\"lazy\\\" src=\\\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig2_HTML.png\\\" width=\\\"685\\\"/></picture><p>SMARCA4 inhibition suppresses the NE phenotype in SCLC. <b>A</b> Hockey-stick plots of DEGs in FHD-286-treated cells after 14 days (100 nM) versus control, untreated cells. (See Table S1). <b>B</b> Dot plots showing negative enrichment in selected neuronal and NE pathways analyzed by GSEA in RNAseq data from H82 and H146 cell lines treated with FHD-286 versus untreated. (See Table S1). <b>C</b> GSEA applying Zhang et al. NE gene signature [28] in H82 cell line treated with FHD-286 versus untreated. <b>D</b> Heatmaps showing the most significant confident targets (top 25 with TPMs > 2) of NEUROD1 (left) and ASCL1 (right) [7], in H82 (left) and H146 (right) bulk RNAseq (FHD-286 treated vs untreated). <b>E</b> Log<sub>2</sub> fold change of Hippo pathway genes from data in A. Student’s two-tailed unpaired t test. ***<i>p</i> < 0.001, **<i>p</i> < 0.01. The mean ± SD is shown. <b>F</b> Log<sub>2</sub> fold change of NOTCH pathway genes from data in <b>A</b>. Student’s two-tailed unpaired t test. ***<i>p</i> < 0.001, *<i>p</i> < 0.05. The mean ± SD is shown. <b>G</b> Western blotting of H524 (SCLC-N), H82 (SCLC-N), HCC33 (SCLC-N), H69 (SCLC-A), SHP77 (SCLC-A) and H146 (SCLC-A) cells after treatment with 100 nM of FHD-286 for 7 and 14 days.<b> H</b> t-SNE of Zhang NE signature and <i>SMARCA4</i> levels applied to public scRNAseq data of 4 myc-driven murine (RPM) tumors [6]. <b>I</b> Scoring for Zhang NE signature and <i>SMARCA4</i> projected in a pseudotime trajectory from early to late time points in a tumor from a Myc-driven murine SCLC model showing subtype plasticity [6]. See also Figs. S2, S3 and Table S1</p><span>Full size image</span><svg aria-hidden=\\\"true\\\" focusable=\\\"false\\\" height=\\\"16\\\" role=\\\"img\\\" width=\\\"16\\\"><use xlink:href=\\\"#icon-eds-i-chevron-right-small\\\" xmlns:xlink=\\\"http://www.w3.org/1999/xlink\\\"></use></svg></figure><figure><figcaption><b data-test=\\\"figure-caption-text\\\">Fig. 3</b></figcaption><picture><source srcset=\\\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig3_HTML.png?as=webp\\\" type=\\\"image/webp\\\"/><img alt=\\\"figure 3\\\" aria-describedby=\\\"Fig3\\\" height=\\\"768\\\" loading=\\\"lazy\\\" src=\\\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig3_HTML.png\\\" width=\\\"685\\\"/></picture><p>SMARCA4 inactivation alters chromatin accessibility in NE-high SCLC.<b> A</b> Heatmap showing ATACseq chromatin accessibility changes (FDR:0.01, FC > 1.5) in H82 and H146 cells after treatment with FHD-286 (100 nM, 14 days). <b>B</b> Enrichment of neuronal and NE HOMER transcription factor-binding DNA motifs in ATAC-seq peaks lost after treatment with FHD-286 (100 nM, 14 days). The percentage indicates the amount of target sequences with motif. <b>C</b> Genomic localization of lost and gained accessible sites upon FHD-286 treatment in H82 and H146 cells. <b>D</b> ATACseq genome tracks of <i>NEUROD1</i>, <i>SYP</i> and <i>CHGA</i> in H82 and H146 cells after treatment with FHD-286. Peaks with a significant reduction in chromatin accessibility are indicated with arrows. <b>E</b> Enrich analysis applied to all genes with lost sites (across all gene body) following FHD-286 treatment. Top 10 GO Biological processes enriched are shown. See also Fig. S4</p><span>Full size image</span><svg aria-hidden=\\\"true\\\" focusable=\\\"false\\\" height=\\\"16\\\" role=\\\"img\\\" width=\\\"16\\\"><use xlink:href=\\\"#icon-eds-i-chevron-right-small\\\" xmlns:xlink=\\\"http://www.w3.org/1999/xlink\\\"></use></svg></figure><figure><figcaption><b data-test=\\\"figure-caption-text\\\">Fig. 4</b></figcaption><picture><source srcset=\\\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig4_HTML.png?as=webp\\\" type=\\\"image/webp\\\"/><img alt=\\\"figure 4\\\" aria-describedby=\\\"Fig4\\\" height=\\\"841\\\" loading=\\\"lazy\\\" src=\\\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig4_HTML.png\\\" width=\\\"685\\\"/></picture><p>SMARCA4 binds to neuronal and NE lineage TF genes in SCLC.<b> A</b> Heatmap and metaplot showing<i>SMARCA4</i> binding profile determined by ChIP-seq in 4 NE SCLC PDXs and a pooled input. The range under the map indicates the ChIP-seq signal intensity. <b>B</b> Metaplots of <i>ASCL1</i> and <i>NEUROD1</i> in all PDXs and input. Heatmaps showing the binding of SMARCA4 to ASCL1 and NEUROD1 gene bodies. The range indicates the normalized enrichment along the respective gene regions. <b>C</b> NE lineage TFs and gene promoter proximal regions (within 1 kb of TSS) bound by SMARCA4 in NE SCLC PDXs. <b>D</b> Dot plot of Poly-Enrich analysis applied to SMARCA4 ChIP-seq peaks. Fold enrichment refers to the fold increase in the signal for a particular gene relative to the background signal. The counts refer to the number of genes detected in the ChIP-seq data that are part of the indicated pathways. <b>E</b> Enrich analysis of 617 consensus genes selected by combining RNAseq from Fig. 2 and ChIP-seq data. See also Fig. S5E. <b>F</b> Enrichment analysis of TF-binding motifs in the SMARCA4 ChIP-seq data identified with HOMER. See also Figs. S5, S6 and Table S3</p><span>Full size image</span><svg aria-hidden=\\\"true\\\" focusable=\\\"false\\\" height=\\\"16\\\" role=\\\"img\\\" width=\\\"16\\\"><use xlink:href=\\\"#icon-eds-i-chevron-right-small\\\" xmlns:xlink=\\\"http://www.w3.org/1999/xlink\\\"></use></svg></figure><figure><figcaption><b data-test=\\\"figure-caption-text\\\">Fig. 5</b></figcaption><picture><source srcset=\\\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig5_HTML.png?as=webp\\\" type=\\\"image/webp\\\"/><img alt=\\\"figure 5\\\" aria-describedby=\\\"Fig5\\\" height=\\\"876\\\" loading=\\\"lazy\\\" src=\\\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig5_HTML.png\\\" width=\\\"685\\\"/></picture><p>SMARCA4 regulates SRRM4 expression to control splicing and activation of REST. <b>A</b> Venn diagram of ASCL1 and NEUROD1 published binding targets from Borromeo et al. [7] overlapping with genes downregulated by FHD-286 in H146 and H82 cells. <b>B</b> Western blots of H82 and H146 cells treated with FHD-286 for 14 days. <b>C</b> Metaplot of SMARCA4 ChIP-seq showing SMARCA4 binding to <i>SRRM4</i> in 4 NE SCLC PDXs. Range indicates the fold enrichment with respect the input. ChIP-seq genome tracks at SRRM4 TSS. Graphs were obtained from IGV. <b>D</b> Correlation of <i>SMARCA4</i> and <i>SRRM4</i> mRNA levels in SCLC patients’ database. Spearman correlation. <b>E</b> Correlation analysis of <i>SRRM4</i> and <i>SMARCA4</i> in cancer cell lines retrieved from CCLE. Cell lines with both high <i>SMARCA4</i> and <i>SRRM4</i> mRNA levels are highlighted. <b>F</b> Merged ATAC-seq tracks of H82 and H146 parentals cells and FHD-286 treated cells (day 14) at SRRM4 gene locus visualized with IGV. <b>G</b> Graphical representation of REST genomic regions and spliced isoforms with the binding location of the different primers used for PCR. <b>H</b> PCR analysis of <i>REST</i> splicing isoforms using two pairs of primers (E2F1 + E4R1 and E1F1 + E4R1) that span N3c. <b>I</b> RT-qPCR of REST4 isoforms (S3, S7, S12) in H82, H146 and H524 treated with FHD-286 (14 days) versus untreated cells. The pair of primers E3N3c and E4R2 that recognizes all isoforms including exon N3c was used. Student’s two-tailed unpaired t test. ***<i>p</i> < 0.001. The mean ± SD is shown. <b>J</b> Enrich analysis applied to commonly and significantly downregulated genes in both H146 and H82 (n = 904) cell lines identified in the bulk-RNAseq (Fig. 2). See also Fig. S7</p><span>Full size image</span><svg aria-hidden=\\\"true\\\" focusable=\\\"false\\\" height=\\\"16\\\" role=\\\"img\\\" width=\\\"16\\\"><use xlink:href=\\\"#icon-eds-i-chevron-right-small\\\" xmlns:xlink=\\\"http://www.w3.org/1999/xlink\\\"></use></svg></figure><figure><figcaption><b data-test=\\\"figure-caption-text\\\">Fig. 6</b></figcaption><picture><source srcset=\\\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig6_HTML.png?as=webp\\\" type=\\\"image/webp\\\"/><img alt=\\\"figure 6\\\" aria-describedby=\\\"Fig6\\\" height=\\\"989\\\" loading=\\\"lazy\\\" src=\\\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-024-01609-7/MediaObjects/13045_2024_1609_Fig6_HTML.png\\\" width=\\\"685\\\"/></picture><p>SMARCA4/2 inhibition by FHD-286 induces ERBB signaling and sensitivity to afatinib in SCLC. <b>A</b> Proliferation curves of SCLC-A, -N, -P and -Y SCLC cell lines treated with FHD-286 for 96 h. The mean ± SD is shown. <b>B</b> Tumor growth of Lx151 and Lx95 SCLC PDXs implanted in NSG mice and treated with 1.5 mg/kg BID p.o. of FHD-286. Student’s two-tailed unpaired t test. ***<i>p</i> < 0.001. <b>C</b> IPA analysis on significantly upregulated genes in FHD-286-treated cells versus control untreated cells. <b>D</b> Immunoblot of ERBB family proteins in H146 and H82 cells after treatment with 100 nM of FHD-286 for 14 days. <b>E</b> Western blots of FHD-286 (100 nM) treated cells at the indicated times. <b>F</b> Synergy plots of FHD-286 and afatinib in NE SCLC cell lines. <b>G</b> Cell death quantification by flow cytometry at day 5 of H146 and H82 cells after treatment with FHD-286, afatinib or both. One way ANOVA followed by Bonferroni comparison test. ***<i>p</i> < 0.001, ****<i>p</i> < 0.0001. <b>H</b> Normalized tumor growth of Lx1042 (SCLC-N), Lx1322 (SCLC-P), Lx151 (SCLC-A) and Lx95 (SCLC-A) relative to day 1 of treatment. Two-way ANOVA followed by Bonferroni comparison test. *<i>p</i> < 0.05, **<i>p</i> < 0.01, ***<i>p</i> < 0.001. <b>I</b> Schematic representation of the role of SMARCA4 in sustaining the NE phenotype in SCLC</p><span>Full size image</span><svg aria-hidden=\\\"true\\\" focusable=\\\"false\\\" height=\\\"16\\\" role=\\\"img\\\" width=\\\"16\\\"><use xlink:href=\\\"#icon-eds-i-chevron-right-small\\\" xmlns:xlink=\\\"http://www.w3.org/1999/xlink\\\"></use></svg></figure><h3>Authors and Affiliations</h3><ol><li><p>Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA</p><p>Esther Redin, Harsha Sridhar, Barbara Pereira Mello, Hong Zhong, Vidushi Durani, Amin Sabet, Parvathy Manoj, Álvaro Quintanal-Villalonga & Charles M. Rudin</p></li><li><p>Center for Epigenetics Research, Memorial Sloan Kettering Cancer Center, New York, NY, USA</p><p>Yingqian A. Zhan & Richard P. Koche</p></li><li><p>Precision Pathology Center, Memorial Sloan Kettering Cancer Center, New York, NY, USA</p><p>Irina Linkov</p></li><li><p>Antitumor Assessment Core, Memorial Sloan Kettering Cancer Center, New York, NY, USA</p><p>Juan Qiu & Elisa de Stanchina</p></li><li><p>Weill Cornell Medicine Graduate School of Medical Sciences, New York, NY, USA</p><p>Vidushi Durani & Charles M. Rudin</p></li><li><p>Applied Bioinformatics Core, Weill Cornell Medicine, New York, NY, 10065, USA</p><p>Maider Astorkia & Doron Betel</p></li><li><p>Division of Hematology and Oncology, Department of Medicine, Weill Cornell Medicine, New York, NY, 10065, USA</p><p>Doron Betel</p></li><li><p>Department of Physiology, Biophysics and Systems Biology, Institute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, 10065, USA</p><p>Doron Betel</p></li></ol><span>Authors</span><ol><li><span>Esther Redin</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Harsha Sridhar</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Yingqian A. Zhan</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Barbara Pereira Mello</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Hong Zhong</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Vidushi Durani</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Amin Sabet</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Parvathy Manoj</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Irina Linkov</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Juan Qiu</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Richard P. Koche</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Elisa de Stanchina</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Maider Astorkia</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Doron Betel</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Álvaro Quintanal-Villalonga</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Charles M. Rudin</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li></ol><h3>Corresponding authors</h3><p>Correspondence to Álvaro Quintanal-Villalonga or Charles M. Rudin.</p><h3>Publisher's Note</h3><p>Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.</p><h3>Lead Contact: </h3><p> Charles M. Rudin</p><h3>Additional file 1.</h3><p><b>Open Access</b> This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. 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0-.92-.08-1.33-.25-.41-.16-.77-.4-1.08-.7-.3-.31-.54-.69-.72-1.13-.17-.44-.26-.95-.26-1.52zm4.61-.62c0-.55-.11-.98-.34-1.28-.23-.31-.58-.47-1.06-.47-.41 0-.77.15-1.08.45-.31.29-.5.73-.57 1.3zm3.01 2.23c.31.24.61.43.92.57.3.13.63.2.98.2.38 0 .65-.08.83-.23s.27-.35.27-.6c0-.14-.05-.26-.13-.37-.08-.1-.2-.2-.34-.28-.14-.09-.29-.16-.47-.23l-.53-.22c-.23-.09-.46-.18-.69-.3-.23-.11-.44-.24-.62-.4s-.33-.35-.45-.55c-.12-.21-.18-.46-.18-.75 0-.61.23-1.1.68-1.49.44-.38 1.06-.57 1.83-.57.48 0 .91.08 1.29.25s.71.36.99.57l-.74.98c-.24-.17-.49-.32-.73-.42-.25-.11-.51-.16-.78-.16-.35 0-.6.07-.76.21-.17.15-.25.33-.25.54 0 .14.04.26.12.36s.18.18.31.26c.14.07.29.14.46.21l.54.19c.23.09.47.18.7.29s.44.24.64.4c.19.16.34.35.46.58.11.23.17.5.17.82 0 .3-.06.58-.17.83-.12.26-.29.48-.51.68-.23.19-.51.34-.84.45-.34.11-.72.17-1.15.17-.48 0-.95-.09-1.41-.27-.46-.19-.86-.41-1.2-.68z" fill="#535353"/></g></svg>\\\" width=\\\"57\\\"/><h3>Cite this article</h3><p>Redin, E., Sridhar, H., Zhan, Y.A. <i>et al.</i> Correction: SMARCA4 controls state plasticity in small cell lung cancer through regulation of neuroendocrine transcription factors and REST splicing. <i>J Hematol Oncol</i> <b>17</b>, 89 (2024). https://doi.org/10.1186/s13045-024-01609-7</p><p>Download citation<svg aria-hidden=\\\"true\\\" focusable=\\\"false\\\" height=\\\"16\\\" role=\\\"img\\\" width=\\\"16\\\"><use xlink:href=\\\"#icon-eds-i-download-medium\\\" xmlns:xlink=\\\"http://www.w3.org/1999/xlink\\\"></use></svg></p><ul data-test=\\\"publication-history\\\"><li><p>Published<span>: </span><span><time datetime=\\\"2024-09-29\\\">29 September 2024</time></span></p></li><li><p>DOI</abbr><span>: </span><span>https://doi.org/10.1186/s13045-024-01609-7</span></p></li></ul><h3>Share this article</h3><p>Anyone you share the following link with will be able to read this content:</p><button data-track=\\\"click\\\" data-track-action=\\\"get shareable link\\\" data-track-external=\\\"\\\" data-track-label=\\\"button\\\" 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更正:Journal of Hematology & Oncology (2024) 17:58 https://doi.org/10.1186/s13045-024-01572-3The 由于在校对阶段文件传输错误,原文错误地遗漏了文章图表中的许多元素。图1SMARCA4表达与SCLC的NE特征相关。A 使用癌症细胞系百科全书(CCLE)评估了来自 30 种肿瘤类型的细胞系的 SMARCA4 mRNA 水平。条形图表示每种肿瘤类型的中位表达量。B 从 Quintanal Villalonga 等人[27]处获取的 LUAD 和 SCLC 标本中的 SMARCA4 mRNA 水平。学生双尾非配对 t 检验。**P < 0.01。C Rudin 等人和 George 等人数据库以及 CCLE[25, 26]中 SYP、CHGA、INSM1、YAP1 和 REST 与 SMARCA4 mRNA 水平的 Spearman 相关性。D 细胞系(CCLE)和临床标本(Rudin等人和George等人)中低NE和高NE SCLC肿瘤的SMARCA4 mRNA表达[25, 26]。单因素方差分析检验,然后进行Bonferroni事后检验。****p < 0.0001, ***p < 0.001, **p < 0.01。E 在表达针对 SMARCA4 和/或 SMARCA2 的不同 shRNA 组合的 H82 和 H146 异源细胞系中对 ASCL1、NEUROD1、SYP 和 CHGA 进行 Western 印迹。来自 E 的 shRNAs 的表达受多西环素处理的影响。多西环素处理 14 天后进行蛋白质收集和印迹。另见图 S1Full size image图 2SMARCA4 抑制 SCLC 的 NE 表型。A FHD-286 处理 14 天(100 nM)后细胞中 DEGs 的曲棍球图与对照组、未处理细胞的曲棍球图。(见表 S1)。B 点阵图显示,在用FHD-286处理的H82和H146细胞系与未处理的细胞系的RNAseq数据中,通过GSEA分析的选定神经元和NE通路的负富集(见表S1)。(见表 S1)。C GSEA应用Zhang等人的NE基因特征[28]分析FHD-286治疗与未治疗的H82细胞株。D 热图显示了 H82(左)和 H146(右)大量 RNAseq(FHD-286 处理与未处理)中 NEUROD1(左)和 ASCL1(右)[7] 最重要的可信靶标(前 25 个,TPMs > 2)。学生双尾非配对 t 检验。***p < 0.001,**p < 0.01。显示的是平均值 ± SD。F A 中数据中 NOTCH 通路基因的对数折叠变化。***p < 0.001,*p < 0.05。显示的是平均值 ± SD。G 用 100 nM 的 FHD-286 处理 H524 (SCLC-N)、H82 (SCLC-N)、HCC33 (SCLC-N)、H69 (SCLC-A)、SHP77 (SCLC-A) 和 H146 (SCLC-A) 细胞 7 天和 14 天后的 Western 印迹。H 应用于 4 个霉菌驱动的小鼠(RPM)肿瘤的公开 scRNAseq 数据的 Zhang NE 特征和 SMARCA4 水平的 t-SNE [6]。I 张NE特征和SMARCA4的评分投影在一个显示亚型可塑性的Myc驱动小鼠SCLC模型肿瘤从早期到晚期时间点的伪时间轨迹上[6]。另见图 S2、S3 和表 S1全尺寸图像图 3SMARCA4 失活改变了 NE-高 SCLC 的染色质可及性。A 热图显示 FHD-286 处理(100 nM,14 天)后 H82 和 H146 细胞中 ATACseq 染色质可及性的变化(FDR:0.01, FC > 1.5)。B FHD-286(100 nM,14 天)处理后 ATAC-seq 峰丢失的神经元和 NE HOMER 转录因子结合 DNA 基序的富集。百分比表示目标序列中含有motif的数量。C FHD-286 处理 H82 和 H146 细胞后丢失和获得的可访问位点的基因组定位。D FHD-286 处理后 H82 和 H146 细胞中 NEUROD1、SYP 和 CHGA 的 ATACseq 基因组轨迹。箭头所示为染色质可及性明显降低的峰值。E 对 FHD-286 处理后丢失位点的所有基因(所有基因体)进行富集分析。图中显示了富集的前 10 个 GO 生物过程。图 4SMARCA4 与 SCLC 中的神经元和 NE 系 TF 基因结合。热图和图谱显示了通过 ChIP-seq 确定的 4 个 NE SCLC PDX 和汇集输入的 SMARCA4 结合概况。图下的范围表示 ChIP-seq 信号强度。B 所有 PDX 和输入中 ASCL1 和 NEUROD1 的图谱。热图显示 SMARCA4 与 ASCL1 和 NEUROD1 基因体的结合情况。范围表示沿相应基因区域的归一化富集。C NE SCLC PDXs 中与 SMARCA4 结合的 NE 系 TFs 和基因启动子近端区域(TSS 的 1 kb 范围内)。应用于 SMARCA4 ChIP-seq 峰的 Poly-Enrich 分析的点阵图。折富集是指特定基因信号相对于背景信号的增加倍数。计数指的是 ChIP-seq 数据中检测到的属于指定通路的基因数量。E 结合图 2 中的 RNAseq 和 ChIP-seq 数据选出的 617 个共识基因的富集分析。另见图 S5E。 F 利用 HOMER 鉴定的 SMARCA4 ChIP-seq 数据中 TF 结合基序的富集分析。另见图 S5、S6 和表 S3Full size image图 5SMARCA4 调节 SRRM4 的表达以控制剪接和激活 REST。A ASCL1和NEUROD1与FHD-286在H146和H82细胞中下调的基因重叠的Borromeo等人[7]发表的结合靶点的维恩图。B 用 FHD-286 处理 14 天的 H82 和 H146 细胞的 Western 印迹。C SMARCA4 ChIP-seq 图谱显示 4 个 NE SCLC PDX 中 SMARCA4 与 SRRM4 结合。范围表示相对于输入的富集倍数。SRRM4 TSS 处的 ChIP-seq 基因组轨迹。图表来自 IGV。D SCLC 患者数据库中 SMARCA4 和 SRRM4 mRNA 水平的相关性。斯皮尔曼相关性。E 从 CCLE 中检索到的癌细胞系中 SRRM4 和 SMARCA4 的相关性分析。同时具有高 SMARCA4 和 SRRM4 mRNA 水平的细胞系突出显示。F 合并 H82 和 H146 亲代细胞以及 FHD-286 处理细胞(第 14 天)在 SRRM4 基因位点的 ATAC-seq 追踪,用 IGV 可视化。G REST 基因组区域和剪接异构体与用于 PCR 的不同引物结合位置的图示。H 使用跨越 N3c 的两对引物(E2F1 + E4R1 和 E1F1 + E4R1)对 REST 剪接异构体进行 PCR 分析。I 用 FHD-286 处理 H82、H146 和 H524(14 天)与未处理细胞中 REST4 同工酶(S3、S7、S12)的 RT-qPCR 检测。使用的引物 E3N3c 和 E4R2 可识别包括 N3c 外显子在内的所有同工酶异构体。学生双尾非配对 t 检验。***p < 0.001。显示的是平均值 ± SD。J Enrich 分析适用于批量 RNAseq 中确定的 H146 和 H82(n = 904)细胞系中常见的显著下调基因(图 2)。另见图 S7Full size imageFig. 6SMARCA4/2 inhibition by FHD-286 induces ERBB signaling and sensitivity to afatinib in SCLC.A FHD-286 处理 SCLC-A、-N、-P 和 -Y SCLC 细胞系 96 小时的增殖曲线。B Lx151 和 Lx95 SCLC PDXs 植入 NSG 小鼠并接受 1.5 mg/kg BID p.o. 的 FHD-286 治疗后的肿瘤生长情况。学生双尾非配对 t 检验。***p < 0.001。C FHD-286 处理过的细胞与未处理过的对照细胞中明显上调基因的 IPA 分析。D 100 nM FHD-286 处理 14 天后 H146 和 H82 细胞中 ERBB 家族蛋白的免疫印迹。E FHD-286 (100 nM) 处理过的细胞在指定时间的 Western 印迹。F FHD-286 和阿法替尼在 NE SCLC 细胞系中的协同作用图。G FHD-286、阿法替尼或两者同时处理 H146 和 H82 细胞后第 5 天的流式细胞术细胞死亡定量。单向方差分析,然后进行 Bonferroni 比较检验。***p < 0.001,****p < 0.0001。H Lx1042(SCLC-N)、Lx1322(SCLC-P)、Lx151(SCLC-A)和Lx95(SCLC-A)相对于治疗第1天的肿瘤生长归一化。双向方差分析,然后进行 Bonferroni 比较检验。*p < 0.05, **p < 0.01, ***p < 0.001。I SMARCA4在维持SCLC的NE表型中的作用示意图全尺寸图片作者及工作单位美国纽约斯隆凯特琳纪念癌症中心医学系Esther Redin, Harsha Sridhar, Barbara Pereira Mello, Hong Zhong, Vidushi Durani, Amin Sabet, Parvathy Manoj, Álvaro Quintanal-Villalonga & Charles M..RudinCenter for Epigenetics Research,Memorial Sloan Kettering Cancer Center,New York,NY,USAYingqian A. Zhan &;Richard P.KochePrecision Pathology Center, Memorial Sloan Kettering Cancer Center, New York, NY, USAIrina LinkovAntitumor Assessment Core, Memorial Sloan Kettering Cancer Center, New York, NY, USAJuan Qiu & Elisa de StanchinaWeill Cornell Medicine Graduate School of Medical Sciences, New York, NY, USAVidushi Durani & Charles M.RudinApplied Bioinformatics Core, Weill Cornell Medicine, New York, NY, 10065, USAMaider Astorkia &;Doron BetelDivision of Hematology and Oncology, Department of Medicine, Weill Cornell Medicine, New York, NY, 10065, USDoron BetelDepartment of Physiology, Biophysics and Systems Biology, Institute for Computational Biomedicine, Weill Cornell Medicine、New York, NY, 10065, USADoron Betel作者Esther Redin查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Harsha Sridhar查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Yingqian A. You can also search for this author.
Correction: SMARCA4 controls state plasticity in small cell lung cancer through regulation of neuroendocrine transcription factors and REST splicing
Correction: Journal of Hematology & Oncology (2024) 17:58 https://doi.org/10.1186/s13045-024-01572-3
The original article mistakenly omitted numerous elements from the article figures due to an error in transferring the files at the proofing stage. The figures have since been updated to restore all missing elements of each affected figure (Figs. 1, 2, 3, 4, 5, 6).
Authors and Affiliations
Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA
Esther Redin, Harsha Sridhar, Barbara Pereira Mello, Hong Zhong, Vidushi Durani, Amin Sabet, Parvathy Manoj, Álvaro Quintanal-Villalonga & Charles M. Rudin
Center for Epigenetics Research, Memorial Sloan Kettering Cancer Center, New York, NY, USA
Yingqian A. Zhan & Richard P. Koche
Precision Pathology Center, Memorial Sloan Kettering Cancer Center, New York, NY, USA
Irina Linkov
Antitumor Assessment Core, Memorial Sloan Kettering Cancer Center, New York, NY, USA
Juan Qiu & Elisa de Stanchina
Weill Cornell Medicine Graduate School of Medical Sciences, New York, NY, USA
Vidushi Durani & Charles M. Rudin
Applied Bioinformatics Core, Weill Cornell Medicine, New York, NY, 10065, USA
Maider Astorkia & Doron Betel
Division of Hematology and Oncology, Department of Medicine, Weill Cornell Medicine, New York, NY, 10065, USA
Doron Betel
Department of Physiology, Biophysics and Systems Biology, Institute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, 10065, USA
Doron Betel
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Redin, E., Sridhar, H., Zhan, Y.A. et al. Correction: SMARCA4 controls state plasticity in small cell lung cancer through regulation of neuroendocrine transcription factors and REST splicing. J Hematol Oncol17, 89 (2024). https://doi.org/10.1186/s13045-024-01609-7
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