Biochimica et biophysica acta. Molecular cell research最新文献_第9页

KLF5 inhibition initiates epithelial-mesenchymal transition in non-transformed human squamous epithelial cells 抑制 KLF5 可启动未转化的人类鳞状上皮细胞的上皮-间质转化。

IF 4.6 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2024-06-22 DOI: 10.1016/j.bbamcr.2024.119789

Dharmendra Bhargava, David Rusakow, Wilson Zheng, Silina Awad, Jonathan P. Katz

{"title":"KLF5 inhibition initiates epithelial-mesenchymal transition in non-transformed human squamous epithelial cells","authors":"Dharmendra Bhargava, David Rusakow, Wilson Zheng, Silina Awad, Jonathan P. Katz","doi":"10.1016/j.bbamcr.2024.119789","DOIUrl":"10.1016/j.bbamcr.2024.119789","url":null,"abstract":"<div><p>The transcriptional regulator <em>Krüppel</em>-like factor 5 (KLF5) is highly expressed in squamous epithelial cells of the esophagus. Increased KLF5 activity induces tumorigenesis and promotes metastasis in several cancers, although this function appears to be context-dependent. Here, we demonstrate that acute KLF5 inhibition, both genetically and with the potent KLF5 inhibitor ML264, causes non-transformed human primary esophageal squamous epithelial cells to enter the epithelial to mesenchymal transition (EMT). Moreover, chronic KLF5 inhibition with ML264 leads to the development of cells with a mesenchymal phenotype characterized by the expression of mesenchymal markers and functionally by reduced cell growth and increased migration and cellular invasion. This EMT resulting from chronic KLF5 inhibition is not driven by β-Catenin or TGF-β signaling. Pharmacologically, ML264 inhibits KLF5 by promoting proteasomal-mediated degradation. Taken together, we demonstrate that reduced KLF5 activity reprograms epithelial cells towards a mesenchymal phenotype and enhances their migratory and invasive potential. These findings have potential implications not only for esophageal cancers but also for normal processes such as esophageal tissue repair following injury.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119789"},"PeriodicalIF":4.6,"publicationDate":"2024-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141442000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Fe-S cluster biosynthesis and maturation: Mass spectrometry-based methods advancing the field Fe-S 簇的生物合成和成熟：基于质谱的方法推动该领域的发展。

IF 4.6 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2024-06-20 DOI: 10.1016/j.bbamcr.2024.119784

Shelby D. Oney-Hawthorne, David P. Barondeau

引用次数: 0

Structural aspects of iron‑sulfur protein biogenesis: An NMR view 铁硫蛋白生物生成的结构问题：核磁共振视图

IF 4.6 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2024-06-18 DOI: 10.1016/j.bbamcr.2024.119786

Leonardo Querci , Mario Piccioli , Simone Ciofi-Baffoni , Lucia Banci

引用次数: 0

Vimentin, inversely correlating with infiltration of CD8 + T lymphocytes, promotes nuclear translocation of PD-L1 in esophageal squamous cell carcinoma 与 CD8 + T 淋巴细胞浸润成反比的波形蛋白可促进食管鳞状细胞癌中 PD-L1 的核易位。

IF 4.6 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2024-06-18 DOI: 10.1016/j.bbamcr.2024.119781

Yan Liang , Shuo He , Qing Liu , Tao Liu , Yiyi Tan , Tianyuan Peng , Conggai Huang , Xiaomei Lu , Shutao Zheng

{"title":"Vimentin, inversely correlating with infiltration of CD8 + T lymphocytes, promotes nuclear translocation of PD-L1 in esophageal squamous cell carcinoma","authors":"Yan Liang , Shuo He , Qing Liu , Tao Liu , Yiyi Tan , Tianyuan Peng , Conggai Huang , Xiaomei Lu , Shutao Zheng","doi":"10.1016/j.bbamcr.2024.119781","DOIUrl":"10.1016/j.bbamcr.2024.119781","url":null,"abstract":"<div><p>Vimentin has been considered a canonical marker of epithelial-mesenchymal transition (EMT) and is associated with tumor escape characterized by aberrant PD-L1 expression. However, whether there is a relationship between vimentin and PD-L1 in esophageal squamous cell carcinoma (ESCC) remains poorly understood. The immunological involvement of vimentin in ESCC was first analyzed by multiplex immunofluorescence staining in ESCC tissue microarray followed by a xenografted mouse model. <em>In vivo</em>, C57BL/6 mice were subcutaneously transplanted with AKR cells after stable silencing of vimentin. <em>In vivo</em> results showed that in addition to PD-L1 and PD-L2 expression, vimentin expression was inversely correlated with CD8+ T-cell infiltration. Mechanistically, vimentin can directly interact with PD-L1 and promote nuclear translocation of PD-L1 in AKR cells. In addition, SEMA6C, STC-2 and TRAILR2 were identified as cytokines modulated by vimentin. Blockade of STC-2 and TRAILR2 in co-culture with their own primary antibodies was shown to recruit more CD8+ T cells than controls. Together, these data strongly suggest targeting Vimenin to overcome the immune cycle in ESCC.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119781"},"PeriodicalIF":4.6,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141431263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Eml1 promotes axonal growth by enhancing αTAT1-mediated microtubule acetylation Eml1通过增强αTAT1介导的微管乙酰化促进轴突生长。

IF 5.1 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2024-06-17 DOI: 10.1016/j.bbamcr.2024.119770

Yufang Zhang , Tuchen Guan , Zhen Li , Beibei Guo , Xiaoqian Luo , Longyu Guo , Mingxuan Li , Man Xu , Mei Liu , Yan Liu

{"title":"Eml1 promotes axonal growth by enhancing αTAT1-mediated microtubule acetylation","authors":"Yufang Zhang , Tuchen Guan , Zhen Li , Beibei Guo , Xiaoqian Luo , Longyu Guo , Mingxuan Li , Man Xu , Mei Liu , Yan Liu","doi":"10.1016/j.bbamcr.2024.119770","DOIUrl":"10.1016/j.bbamcr.2024.119770","url":null,"abstract":"<div><p>Microtubule stabilization is critical for axonal growth and regeneration, and many microtubule-associated proteins are involved in this process. In this study, we found that the knockdown of echinoderm microtubule-associated protein-like 1 (EML1) hindered axonal growth in cultured cortical and dorsal root ganglion neurons. We further revealed that EML1 facilitated the acetylation of microtubules and that the impairment of axonal growth due to EML1 inhibition could be restored by treatment with deacetylase inhibitors, suggesting that EML1 affected tubulin acetylation. Moreover, we verified an interaction between EML1 and the alpha-tubulin acetyltransferase 1, which is responsible for the acetylation of alpha-tubulin. We thus proposed that EML1 might regulate microtubule acetylation and stabilization via alpha-tubulin acetyltransferase 1 and then promote axon growth. Finally, we verified that the knockdown of EML1 in vivo also inhibited sciatic nerve regeneration. Our findings revealed a novel effect of EML1 on microtubule acetylation during axonal regeneration.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119770"},"PeriodicalIF":5.1,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141426223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Promoter hypermethylation-induced downregulation of ITGA7 promotes colorectal cancer proliferation and migration by activating the PI3K/AKT/NF-κB pathway 启动子高甲基化诱导的 ITGA7 下调通过激活 PI3K/AKT/NF-κB 通路促进结直肠癌的增殖和迁移

IF 5.1 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2024-06-15 DOI: 10.1016/j.bbamcr.2024.119785

Jianjun Wang , Yu Wang , Jijun Zhu , Lili Wang , Yanlin Huang , Huiru Zhang , Xiaoyan Wang , Xiaomin Li

{"title":"Promoter hypermethylation-induced downregulation of ITGA7 promotes colorectal cancer proliferation and migration by activating the PI3K/AKT/NF-κB pathway","authors":"Jianjun Wang , Yu Wang , Jijun Zhu , Lili Wang , Yanlin Huang , Huiru Zhang , Xiaoyan Wang , Xiaomin Li","doi":"10.1016/j.bbamcr.2024.119785","DOIUrl":"10.1016/j.bbamcr.2024.119785","url":null,"abstract":"<div><p>We previously reported that integrin alpha 7 (ITGA7) was downregulated in colorectal cancer (CRC) tissues and CRC cell lines and that the lower expression of ITGA7 in CRC tissues was correlated with distant metastasis, suggesting that ITGA7 may function as a suppressor in CRC. The present research was conducted to further investigate the role and mechanisms of ITGA7 in CRC progression. First, bisulfite modification and genomic sequencing (BSP) results showed that the methylation rate of ITGA7 promoter was higher in 10 CRC tissues than in the matched normal tissues. Additionally, 5-Aza-CdR treatment increased ITGA7 expression in CRC cells. Gain-of-function assays revealed the inhibitory role of ITGA7 in CRC cell proliferation and migration. Mechanistically, RNA sequencing, RT-qPCR, and cytoplasm and nuclear separation and rescue assays indicated that knockdown of ITGA7 activated the transcription of MMP9, SETD7, and ADAM15 by enhancing the nuclear translocation of NF-κB. Moreover, CoIP and Western blot suggested a mechanistic model in which ITGA7 binds to CKAP4 to block the interaction of CKAP4 and PI3K p85α and thereby suppress the PI3K/AKT/NF-κB pathway. Accordingly, the current study suggests that ITGA7 functions as a suppressor in CRC progression and that its expression is controlled by promoter methylation.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119785"},"PeriodicalIF":5.1,"publicationDate":"2024-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141410999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TGF-β2 enhances glycolysis in chondrocytes via TβRI/p-Smad3 signaling pathway TGF-β2 通过 TβRI/p-Smad3 信号通路增强软骨细胞中的糖酵解。

IF 4.6 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2024-06-13 DOI: 10.1016/j.bbamcr.2024.119788

Jieya Wei, Siqun Xu, Yang Liu, Li Zhang, Hao Chen, Jiazhou Li, Mengmeng Duan, Zhixing Niu, Minglei Huang, Demao Zhang, Xuedong Zhou, Jing Xie

{"title":"TGF-β2 enhances glycolysis in chondrocytes via TβRI/p-Smad3 signaling pathway","authors":"Jieya Wei, Siqun Xu, Yang Liu, Li Zhang, Hao Chen, Jiazhou Li, Mengmeng Duan, Zhixing Niu, Minglei Huang, Demao Zhang, Xuedong Zhou, Jing Xie","doi":"10.1016/j.bbamcr.2024.119788","DOIUrl":"10.1016/j.bbamcr.2024.119788","url":null,"abstract":"<div><p>Chondrocytes rely heavily on glycolysis to maintain the metabolic homeostasis and cartilage matrix turnover. Glycolysis in chondrocytes is remodeled by diverse biochemical and biomechanical factors due to the sporty joint microenvironment. Transforming growth factor-β2 (TGF-β2), one of the most abundant TGF-β superfamily members in chondrocytes, has increasingly attracted attention in cartilage physiology and pathology. Although previous studies have emphasized the importance of TGF-β superfamily members on cell metabolism, whether and how TGF-β2 modulates glycolysis in chondrocytes remains elusive. In the current study, we investigated the effects of TGF-β2 on glycolysis in chondrocytes and explored the underlying biomechanisms. The results showed that TGF-β2 could enhance glycolysis in chondrocytes by increasing glucose consumption, up-regulating liver-type ATP-dependent 6-phosphofructokinase (Pfkl) expression, and boosting lactate production. The TGF-β2 signal entered chondrocytes via TGF-β receptor type I (TβRI), and activated p-Smad3 signaling to regulate the glycolytic pathway. Subsequent experiments employing specific inhibitors of TβRI and p-Smad3 further substantiated the role of TGF-β2 in enhancement of glycolysis via TβRI/p-Smad3 axis in chondrocytes. The results provide new understanding of the metabolic homeostasis in chondrocytes induced by TGF-β superfamily and might shed light on the prevention and treatment of related osteoarticular diseases.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119788"},"PeriodicalIF":4.6,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141327193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

WhiB-like proteins: Diversity of structure, function and mechanism WhiB 样蛋白：结构、功能和机制的多样性

IF 5.1 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2024-06-13 DOI: 10.1016/j.bbamcr.2024.119787

Daisy Guiza Beltran , Tao Wan , LiMei Zhang

引用次数: 0

Expression of a kinase inactive SLK is embryonic lethal and impairs cell migration in fibroblasts 表达无激酶活性的 SLK 会导致胚胎死亡，并影响成纤维细胞的迁移。

IF 5.1 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2024-06-12 DOI: 10.1016/j.bbamcr.2024.119783

Samuel V. Delisle , Cedrik Labreche , Mónica Lara-Márquez , John Abou-Hamad , Brennan Garland , Nathalie Lamarche-Vane , Luc A. Sabourin

{"title":"Expression of a kinase inactive SLK is embryonic lethal and impairs cell migration in fibroblasts","authors":"Samuel V. Delisle , Cedrik Labreche , Mónica Lara-Márquez , John Abou-Hamad , Brennan Garland , Nathalie Lamarche-Vane , Luc A. Sabourin","doi":"10.1016/j.bbamcr.2024.119783","DOIUrl":"10.1016/j.bbamcr.2024.119783","url":null,"abstract":"<div><p>Kinases are known to have kinase activity independent functions. To gain further insights into potential kinase-independent functions of SLK/STK2, we have developed a kinase-dead allele, SLK<sup>K63R</sup> using <em>in vivo</em> CRISPR/Cas technology. Our studies show that blastocysts homozygote for SLK<sup>K63R</sup> do not develop into viable mice. However, heterozygotes are viable and fertile with no overt phenotypes. Analyses of mouse embryonic fibroblasts show that expression of SLK<sup>K63R</sup> results in a 50% decrease in kinase activity in heterozygotes. In contrast to previous studies, our data show that SLK does not form homodimers and that the kinase defective allele does not act in a dominant negative fashion. Expression of SLK<sup>K63R</sup> leads to altered Rac1 and RhoA activity, increased stress fiber formation and delayed focal adhesion turnover. Our data support a previously observed role for SLK in cell migration and suggest that at least 50% kinase activity is sufficient for embryonic development.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119783"},"PeriodicalIF":5.1,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141316686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of circadian gene CLOCK in cancer 昼夜节律基因 CLOCK 在癌症中的作用。

IF 5.1 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2024-06-12 DOI: 10.1016/j.bbamcr.2024.119782

Nasot Rashed , Wenbin Liu , Xinran Zhou , Ann M. Bode , Xiangjian Luo

引用次数: 0