Molecular Cancer最新文献

{"title":"Wnt signaling in cancer: from biomarkers to targeted therapies and clinical translation","authors":"Muhammad Tufail, Can-Hua Jiang, Ning Li","doi":"10.1186/s12943-025-02306-w","DOIUrl":"https://doi.org/10.1186/s12943-025-02306-w","url":null,"abstract":"The Wnt signaling pathway plays a crucial role in development and tissue homeostasis, regulating key cellular processes such as proliferation, differentiation, and apoptosis. However, its abnormal activation is strongly associated with tumorigenesis, metastasis, and resistance to therapy, making it a vital target for cancer treatment. This review provides a comprehensive insight into the role of Wnt signaling in cancer, examining its normal physiological functions, dysregulation in malignancies, and therapeutic potential. We emphasize the importance of predicting Wnt signaling sensitivity and identify key biomarkers across various cancer types. Additionally, we address the challenges and future prospects of Wnt-targeted therapies, including biomarker discovery, advancements in emerging technologies, and their application in clinical practice.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"3 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143757996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Tetrathiomolybdate inhibits head and neck cancer metastasis by decreasing tumor cell motility, invasiveness and by promoting tumor cell anoikis","authors":"Pawan Kumar, Arti Yadav, Samip N. Patel, Mozaffarul Islam, Quintin Pan, Sofia D. Merajver, Theodoros N. Teknos","doi":"10.1186/s12943-025-02316-8","DOIUrl":"https://doi.org/10.1186/s12943-025-02316-8","url":null,"abstract":"<p><b>Retraction Note: </b><b><i>Mol Cancer </i></b><b>9, 206 (2010)</b></p><p><b>https://doi.org/10.1186/1476-4598-9-206</b></p><p>The Editor-in-Chief has retracted this article. After publication, concerns were raised regarding highly similar images between this article and the authors’ earlier publication [1]. Specifically, Fig. 5A TM- image in this article appears to overlap with Fig. 6C UM-SCC-74 A + EC-Bcl-2 in [1], and Fig. 5A TM + image appears to overlap with Fig. 6C UM-SCC-74 A + EC-VC and UM-SCC-74 A + EC-Bcl-2 + α-IL-8 images in [1]. In addition, Fig. 1C EC-VC + TM and EC-Bcl-2 + TM images appear to overlap.</p><p>The Editor-in-Chief therefore no longer has confidence in the presented data.</p><p>The authors have not responded to any correspondence from the editor or publisher about this retraction.</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Kumar P, Ning Y, Polverini PJ. Endothelial cells expressing Bcl-2 promotes tumor metastasis by enhancing tumor angiogenesis, blood vessel leakiness and tumor invasion. Lab Invest. 2008;88(7):740–9. https://doi.org/10.1038/labinvest.2008.46.</p><p>Article CAS PubMed Google Scholar </p></li></ol><p>Download references<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><h3>Authors and Affiliations</h3><ol><li><p>Department of Otolaryngology-Head and Neck Surgery and Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA</p><p>Pawan Kumar, Arti Yadav, Mozaffarul Islam, Quintin Pan & Theodoros N. Teknos</p></li><li><p>Department of Otolaryngology-Head and Neck Surgery, University of South Florida, Tampa, FL, USA</p><p>Samip N. Patel</p></li><li><p>Department of Internal Medicine, Division of Hematology and Oncology, University of Michigan, Ann, Arbor, MI, USA</p><p>Sofia D. Merajver</p></li></ol><span>Authors</span><ol><li><span>Pawan Kumar</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Arti Yadav</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Samip N. Patel</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Mozaffarul Islam</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Quintin Pan</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Sofia D. Merajver</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></l","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"37 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"C1Q+ TPP1+ macrophages promote colon cancer progression through SETD8-driven p53 methylation","authors":"Veronica Veschi, Francesco Verona, Sebastiano Di Bella, Alice Turdo, Miriam Gaggianesi, Simone Di Franco, Laura Rosa Mangiapane, Chiara Modica, Melania Lo Iacono, Paola Bianca, Ornella Roberta Brancato, Caterina D’Accardo, Gaetana Porcelli, Vincenzo Luca Lentini, Isabella Sperduti, Elisabetta Sciacca, Peter Fitzgerald, David Lopez-Perez, Pierre Martine, Kate Brown, Giuseppe Giannini, Ettore Appella, Giorgio Stassi, Matilde Todaro","doi":"10.1186/s12943-025-02293-y","DOIUrl":"https://doi.org/10.1186/s12943-025-02293-y","url":null,"abstract":"In many tumors, the tumor suppressor TP53 is not mutated, but functionally inactivated. However, mechanisms underlying p53 functional inactivation remain poorly understood. SETD8 is the sole enzyme known to mono-methylate p53 on lysine 382 (p53K382me1), resulting in the inhibition of its pro-apoptotic and growth-arresting functions. We analyzed SETD8 and p53K382me1 expression in clinical colorectal cancer (CRC) and inflammatory bowel disease (IBD) samples. Histopathological examinations, RNA sequencing, ChIP assay and preclinical in vivo CRC models, were used to assess the functional role of p53 inactivation in tumor cells and immune cell infiltration. By integrating bulk RNAseq and scRNAseq approaches in CRC patients, SETD8-mediated p53 regulation resulted the most significantly enriched pathway. p53K382me1 expression was confined to colorectal cancer stem cells (CR-CSCs) and C1Q+ TPP1+ tumor-associated macrophages (TAMs) in CRC patient tissues, with high levels predicting decreased survival probability. TAMs promote p53 functional inactivation in CR-CSCs through IL-6 and MCP-1 secretion and increased levels of CEBPD, which directly binds SETD8 promoter thus enhancing its transcription. The direct binding of C1Q present on macrophages and C1Q receptor (C1QR) present on cancer stem cells mediates the cross-talk between the two cell compartments. As monotherapy, SETD8 genetic and pharmacological (UNC0379) inhibition affects the tumor growth and metastasis formation in CRC mouse avatars, with enhanced effects observed when combined with IL-6 receptor targeting. These findings suggest that p53K382me1 may be an early step in tumor initiation, especially in inflammation-induced CRC, and could serve as a functional biomarker and therapeutic target in adjuvant setting for advanced CRCs. ","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"183 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143736599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: SPOCK1 as a potential cancer prognostic marker promotes the proliferation and metastasis of gallbladder cancer cells by activating the PI3K/AKT pathway","authors":"Yi-Jun Shu, Hao Weng, Yuan-Yuan Ye, Yun-Ping Hu, Run-Fa Bao, Yang Cao, Xu-An Wang, Fei Zhang, Shan-Shan Xiang, Huai-Feng Li, Xiang-Song Wu, Mao-Lan Li, Lin Jiang, Wei Lu, Bao-San Han, Zhi-Gang Jie, Ying-Bin Liu","doi":"10.1186/s12943-025-02313-x","DOIUrl":"https://doi.org/10.1186/s12943-025-02313-x","url":null,"abstract":"<p><b>Correction: Mol Cancer 14, 12 (2015)</b></p><p><b>https://doi.org/10.1186/s12943-014-0276-y</b></p><br/><p>Following publication of the original article [1], the author has requested the publication of an erratum to address the following issues stated below.</p><p>Recently, in planning and designing further studies of the roles of SPOCK1 in chemo-resistance of gallbladder cancer, based on the authors ‘ previous investigations including the above mentioned paper, they noticed an error in the Fig. 5 A&B. They found that in Fig. 5A, the pictures of NOZ cells in the shSPOCK1 group were placed incorrectly and in Fig. 5B, the pictures of SGC cells in the Mock group were placed incorrectly. There errors likely resulted from incorporation of the incorrect figure panels due to the high similarities of both file names and images from the repeated experiments in the original data folder. However, these errors in the images do not affect any statistical results and the relevant conclusions. They have carefully examined the original results and now the incorrect Fig. 5 and correct Fig. 5 are povided below.</p><p>Incorrect Fig. 5:</p><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%2Fs12943-025-02313-x/MediaObjects/12943_2025_2313_Fig1_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 1\" aria-describedby=\"Fig1\" height=\"1016\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02313-x/MediaObjects/12943_2025_2313_Fig1_HTML.png\" width=\"685\"/></picture><p>SPOCK1 promotes tumor invasion and metastasis <i>in vitro</i> by inducing EMT.<b> A</b> Wound closure was delayed in Lv-shSPOCK1-transduced cells compared with that in CTRL and Lv-shNC cells at 48 h in both GBC-SD and NOZ cells. Overexpression of SPOCK1 in SGC-996 cells had the opposite effects (*<i>P</i> < 0.05, *<i>*P</i> < 0.01, and ***<i>P</i> < 0.001). <b>B</b> Matrigel invasion assay of CTRL, Lv-shNC, Lv-shSPOCK1, MOCK, and SPOCK1 transfectants cells. The number of invaded cells was calculated and is depicted in the bar chart. (*<i>P</i> < 0.05, **<i>P</i> < 0.01, and ***<i>P</i> < 0.001). <b>C </b>and<b> D</b> The protein expression of Snail, vimentin, N-cadherin and E-cadherin in the indicated cells was examined by western blotting. The protein expression of vementin and E-cadherin was examined by immunofluorescence analysis. The red signal represents staining for E-cadherin or vimentin. Nuclei were counterstained with DAPI</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><p>Correct Fig. 5:</p><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 5</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springe","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"38 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143736603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial expression of concern: Withanolide D induces apoptosis in leukemia by targeting the activation of neutral sphingomyelinase-ceramide cascade mediated by synergistic activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase","authors":"Susmita Mondal, Chandan Mandal, Rajender Sangwan, Sarmila Chandra, Chitra Mandal","doi":"10.1186/s12943-024-02185-7","DOIUrl":"https://doi.org/10.1186/s12943-024-02185-7","url":null,"abstract":"<p><b>Correction:</b> <b><i>Mol Cancer</i></b> <b>9, 239 (2010)</b></p><p><b>https://doi.org/10.1186/1476-4598-9-239</b></p><p>The Editor-in-Chief is issuing this editorial expression of concern to inform the readers that following the publication of the article, concerns were raised regarding multiple image similarities found in Figs. 1B and E and 2C, 3 A, 4 A, 5 A, and 7E. Due to the age of the article, the authors were unable to provide all concerned raw data files. An investigation by the publisher found evidence of image editing that was not transparently stated in the article. Additionally, the flow cytometry plot in Fig. 1e shows repetitive data point patterns, which are unlikely to occur naturally in this type of data. Similarly, the background of the blot presented in Fig. 2c appears to show repetitive non-specific markings.</p><p>Therefore readers are alerted to interpret this data with caution.</p><p>Author, Chitra Mandal agrees with this Editorial Express of Concern. The Publisher is unable to get current email addresses for authors, Susmita Mondal, Chandan Mandal, Rajender Sangwan, and Sarmila Chandra.</p><h3>Authors and Affiliations</h3><ol><li><p>Infectious diseases and immunology Division, Indian Institute of Chemical Biology, A Unit of Council of Scientific and Industrial Research, Govt. of India, 4, Raja S. C. Mullick Road, Kolkata, 700032, India</p><p>Susmita Mondal, Chandan Mandal & Chitra Mandal</p></li><li><p>Central Institute of Medicinal and Aromatic Plants, Lucknow, 226015, India</p><p>Rajender Sangwan</p></li><li><p>Kothari Medical Center, 8/3, Alipore Road, Kolkata, 700027, India</p><p>Sarmila Chandra</p></li><li><p>Department of Microbiology, Sammilani Mahavidyalaya, Baghajatin, E.M By Pass, Kolkata, 700075, India</p><p>Susmita Mondal</p></li></ol><span>Authors</span><ol><li><span>Susmita Mondal</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Chandan Mandal</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Rajender Sangwan</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Sarmila Chandra</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Chitra Mandal</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li></ol><h3>Corresponding author</h3><p>Correspondence to Chitra Mandal.</p><h3>Publisher’s note</h3><p>Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.</p><p>The online version of the original article can be found at https://doi.org/10.1186/1476-4598-9-239.</p><p><b>Open","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"28 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143736600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer neuroscience in head and neck: interactions, modulation, and therapeutic strategies","authors":"Hanrui Wang, Xiaoyu Song, Hui Shen, Wanchen Liu, Yao Wang, Mingjun Zhang, Ting Yang, Yakui Mou, Chao Ren, Xicheng Song","doi":"10.1186/s12943-025-02299-6","DOIUrl":"https://doi.org/10.1186/s12943-025-02299-6","url":null,"abstract":"Head and neck cancer (HNC) is an aggressive malignancy with significant effects on the innervation. Not only is it at the top of the cancer spectrum with a dismal prognosis, but it also imposes considerable stress on patients and society owing to frequent neurological symptoms. With progress in cancer neuroscience, the interactions between HNC and the nervous system, as well as the underlying mechanisms, have become increasingly clear. Compelling evidence suggests communication of information between cancer and nerve cells and devastation of the neurological system with tumor growth. However, the thorough grasp of HNC in cancer neuroscience has been severely constrained by the intricacy of HNC and fragmented research. This review comprehensively organizes and summarizes the latest research on the crosstalk between HNC and the nervous system. It aims to clarify various aspects of the neurological system in HNC, including the physiology, progression, and treatment of cancer. Furthermore, the opportunities and challenges of cancer neuroscience in HNC are discussed, which offers fresh perspectives on the neurological aspects of HNC diagnosis and management.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"36 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143736598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating MicroRNAs: functional biomarkers for melanoma prognosis and treatment","authors":"Su Yin Lim, Suzanah C. Boyd, Russell J. Diefenbach, Helen Rizos","doi":"10.1186/s12943-025-02298-7","DOIUrl":"https://doi.org/10.1186/s12943-025-02298-7","url":null,"abstract":"MicroRNAs (miRNAs) hold significant promise as circulating cancer biomarkers and unlike many other molecular markers, they can provide valuable insights that extend beyond tumour biology. The expression of circulating miRNAs may parallel the cellular composition and dynamic activity within the tumour microenvironment and reveal systemic immune responses. The functional complexity of miRNAs—where a single miRNA can regulate multiple messenger RNAs (mRNAs) to fine tune fundamental processes, and a single mRNA can be targeted by multiple miRNAs—underscores their broad significance and impact. However, this complexity poses significant challenges for translating miRNA research into clinical practice. In melanoma, specific miRNA signatures have shown notable diagnostic, prognostic and predictive value, with lineage-specific and immune-related miRNAs frequently identified as valuable markers. In this review, we explore the role of circulating miRNAs as potential biomarkers in melanoma, and highlight the current status and advances required to translate miRNA research into therapeutic opportunities.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"19 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143723162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: CircZBTB44 promotes renal carcinoma progression by stabilizing HK3 mRNA structure","authors":"Tushuai Li, Yue Gu, Baocai Xu, Kamil Kuca, Jie Zhang, Wenda Wu","doi":"10.1186/s12943-025-02307-9","DOIUrl":"https://doi.org/10.1186/s12943-025-02307-9","url":null,"abstract":"<p><b>Correction</b><b>: </b><b>Mol Cancer 22, 77 (2023)</b></p><p><b>https://doi.org/10.1186/s12943-023-01771-5</b></p><br/><p>Following the publication of the original article [1], the authors reported that the EdU staining image for the si-circ1+oe-HK3 group of A549 cell in Figure 7C was mistakenly used. The authors have requested to update the Figure 7. The incorrect and correct Figure 7 are provided below.</p><p>Incorrect Figure 7:</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02307-9/MediaObjects/12943_2025_2307_Figa_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure a\" aria-describedby=\"Figa\" height=\"343\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02307-9/MediaObjects/12943_2025_2307_Figa_HTML.png\" width=\"685\"/></picture></figure><p>Correct Figure 7:</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02307-9/MediaObjects/12943_2025_2307_Figb_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure b\" aria-describedby=\"Figb\" height=\"343\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02307-9/MediaObjects/12943_2025_2307_Figb_HTML.png\" width=\"685\"/></picture></figure><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Li T, Gu Y, Xu B, et al. CircZBTB44 promotes renal carcinoma progression by stabilizing HK3 mRNA structure. Mol Cancer. 2023;22:77. https://doi.org/10.1186/s12943-023-01771-5.</p><p>Article CAS PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<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><h3>Authors and Affiliations</h3><ol><li><p>School of Food and Biological Engineering, Hefei University of Technology, 420 Feicui Road, Hefei, 230009, China</p><p>Tushuai Li, Baocai Xu & Wenda Wu</p></li><li><p>Wuxi School of Medicine, Jiangnan University, Wuxi, 214013, China</p><p>Tushuai Li</p></li><li><p>MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, China</p><p>Tushuai Li & Wenda Wu</p></li><li><p>Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Institute of Clinical Pharmacology, Anhui Medical University, Hefei, 230032, China</p><p>Yue Gu</p></li><li><p>School of Biology and Food Engineering, Changshu Institute of Technology, 99 Southern Sanhuan Road, Suzhou, 215500, China</p><p>Jie Zhang</p></li><li><p>Department of Chemistry, Faculty of Science, University of Hradec Kralove, Hradec Kralove, 50003, Czech Republic</p><p>Kamil Kuca & Wenda Wu</p></li></ol><span>Authors</span><ol><li><span>Tushuai Li</span>View author publicat","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"72 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143713399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunomodulatory gene networks predict treatment response and survival to de-escalated, anthracycline-free neoadjuvant chemotherapy in triple-negative breast cancer in the WSG-ADAPT-TN trial","authors":"Darren Korbie, Clare Stirzaker, Oleg Gluz, Christine zu Eulenburg, Ulrike Nitz, Matthias Christgen, Sherko Kuemmel, Eva-Maria Grischke, Helmut Forstbauer, Michael Braun, Mathias Warm, John Hackmann, Christoph Uleer, Bahriye Aktas, Claudia Schumacher, Rachel Wuerstlein, Enrico Pelz, Hans Heinrich Kreipe, Susan J. Clark, Matt Trau, Monika Graeser, Nadia Harbeck","doi":"10.1186/s12943-025-02275-0","DOIUrl":"https://doi.org/10.1186/s12943-025-02275-0","url":null,"abstract":"Anthracycline-containing neoadjuvant chemotherapy (NACT) is the standard treatment for early triple-negative breast cancer (eTNBC); however, it is associated with substantial toxicity. We performed whole transcriptome profiling of baseline tumor biopsies to identify gene networks predictive and prognostic for pathological complete response (pCR) and survival after de-escalated, anthracycline-free NACT in the WSG-ADAPT-TN trial (NCT01815242). eTNBC patients (cT1c-cT4c, cN +) were randomized to 12 weeks of nab-paclitaxel + gemcitabine (n = 182) or nab-paclitaxel + carboplatin (n = 154). The primary endpoint was pCR (ypT0/is, ypN0), and the secondary endpoints included survival and translational research. AmpliSeq RNA sequencing, allowing simultaneous analysis of the expression of > 20,000 genes, was performed in 135 patients. Differentially expressed genes were evaluated in training (n = 67) and validation (n = 68) sets, and a polygenic score (PS) for prediction of pCR (PS:pCR) and a PS for prediction of invasive disease-free survival (PS:iDFS) were found. 49/135 (36.3%) patients had pCR; 30 iDFS events occurred during 60-month median follow-up. Immune recruitment and viral defense gene networks were strongly associated with pCR, while metabolic pathways were associated with survival. PS:pCR and PS:iDFS predominantly included immune-related genes. Diagnostic accuracy (ROC AUC) in the validation cohort was 83% for PS:pCR and 64% for PS:iDFS. At optimized cut-off, PS:pCR identified a group with a 67.7% pCR rate (vs. 10.8%; p < .0001), and PS:iDFS detected a group with 79.5% (95%CI 64.1%, 88.8%) 5-year iDFS rate (vs. 55.0%, 95%CI 29.8%, 74.5%; p = .04). Polygenic scores incorporating immunoregulatory genes can predict pCR and survival and represent an opportunity to select patients for de-escalated, anthracycline-free NACT. This transcriptome network analysis also identifies potential new targets for personalized medicine approaches in patients without response to NACT. NCT01815242.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"28 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143702980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of 6-phosphogluconate dehydrogenase suppresses esophageal squamous cell carcinoma growth and enhances the anti-tumor effects of metformin via the AMPK/mTOR pathway","authors":"Bei Wang, Zixuan Wang, Zini Zhou, Gui Liu, Zhenyuan Jiang, Mingyue Zheng, Wei Geng","doi":"10.1186/s12943-025-02302-0","DOIUrl":"https://doi.org/10.1186/s12943-025-02302-0","url":null,"abstract":"Metabolic reprogramming plays a pivotal role in the development and progression of tumors. Tumor cells rely on glycolysis as their primary energy production pathway and effectively utilize biomolecules generated by the pentose phosphate pathway (PPP) for efficient biosynthesis. However, the role of 6-phosphogluconate dehydrogenase (6PGD), a crucial enzyme in the PPP, remains unexplored in esophageal squamous cell carcinoma (ESCC). In this study, we observed a significant upregulation of 6PGD expression in ESCC tissues, which correlated with an unfavorable prognosis among patients. The experiments demonstrated that knockdown of 6PGD induces oxidative stress and suppresses ESCC cell proliferation. Mechanistically, this is achieved through AMPK activation and subsequent inhibition of downstream mTOR phosphorylation. Moreover, physcion has been found to inhibit 6PGD activity and exert its anti-ESCC effect via the AMPK/mTOR pathway. Subsequently, we conducted both in vitro and in vivo experiments to validate the anticancer efficacy of combining metformin, an AMPK activator, with physcion. The results demonstrated a significantly enhanced inhibition of ESCC growth. This study elucidates the impact of 6PGD on ESCC cell proliferation along with its underlying molecular mechanisms, highlighting its potential as a therapeutic target for ESCC. Furthermore, we investigated a novel approach for improved anti-tumor therapy involving physcion and metformin. These findings will contribute new insights to clinical treatment strategies for ESCC while providing a theoretical foundation for developing molecular targeted therapies.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"14 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143702979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}