Biochimica et biophysica acta. Molecular cell research最新文献

Carnosine drives mitochondrial biogenesis and skeletal muscle regeneration via Sirt1-mediated nuclear translocation of PGC-1α. 肌肽通过sirt1介导的PGC-1α核易位驱动线粒体生物发生和骨骼肌再生。

IF 4.3 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-10-15 DOI: 10.1016/j.bbamcr.2026.120237

Yanyan Liang, Chenjin Song, Lei Xing, Yuxin Chen, Huaixin Teng, Bo Tian, Shuang Li, Xin Jin, Huili Tong

{"title":"Carnosine drives mitochondrial biogenesis and skeletal muscle regeneration via Sirt1-mediated nuclear translocation of PGC-1α.","authors":"Yanyan Liang, Chenjin Song, Lei Xing, Yuxin Chen, Huaixin Teng, Bo Tian, Shuang Li, Xin Jin, Huili Tong","doi":"10.1016/j.bbamcr.2026.120237","DOIUrl":"https://doi.org/10.1016/j.bbamcr.2026.120237","url":null,"abstract":"<p><p>Post-injury skeletal muscle regeneration depends on the proliferation and differentiation of satellite cells, and mitochondrial function acts as an essential prerequisite for this biological process. This study shows carnosine promotes mouse C2C12 myoblast proliferation, up-regulates mitochondrial genes, and activates oxidative phosphorylation and ATP synthesis. In mechanism, it promotes PGC-1α nuclear translocation, TFAM expression, mitochondrial biogenesis and ATP production. The pharmacological inhibition of Sirt1 by EX-527 eliminated the nuclear accumulation of Sirt1 and PGC-1α induced by carnosine, which confirmed that Sirt1 is an important mediator. Animal experiments confirmed that oral carnosine could accelerate the repair of injury, increase regenerated muscle fibers on the 7th day, and up regulate Pax7, myogenic differentiation 1 (MyoD) and myogenin (MyoG). Molecular docking showed that carnosine could bind to Sirt1 protein. This study clarified that carnosine can drive mitochondrial biogenesis by targeting Sirt1/PGC-1α/TFAM signaling axis, thus promoting myogenesis and muscle repair, providing a theoretical basis for the clinical application of carnosine.</p>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":" ","pages":"120237"},"PeriodicalIF":4.3,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190866","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

Retraction notice to "Compression regulates gene expression of chondrocytes through HDAC4 nuclear relocation via PP2A-depended HDAC4 dephosphorylation" [Biochimica et Biophysica Acta (BBA) - Mol. Cell Res. 1863 (2016) 1633-1642]. “压缩通过pp2a依赖的HDAC4去磷酸化调控HDAC4核重定位软骨细胞的基因表达”[biochemica et Biophysica Acta (BBA) - Mol. Cell Res. 1863(2016) 1633-1642]。

IF 4.3 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-10-12 DOI: 10.1016/j.bbamcr.2026.120189

Chongwei Chen, Xiaochun Wei, Shaowei Wang, Qiang Jiao, Yang Zhang, Guoqing Du, Xiaohu Wang, Fangyuan Wei, Jianzhong Zhang, Lei Wei

引用次数: 0

DLL1 promotes diabetic cataract progression by driving epithelial-mesenchymal transition (EMT) via activation of the Notch signaling pathway. DLL1通过激活Notch信号通路，驱动上皮-间质转化（EMT），从而促进糖尿病性白内障的进展。

IF 4.3 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-10-09 DOI: 10.1016/j.bbamcr.2026.120233

Yuanyuan Wang, Jiquan Wen, Tingting Zhu, Xiangming Zha, Chengcheng Fang, Zhen Li, Lijun Shen, Tingjun Xu

{"title":"DLL1 promotes diabetic cataract progression by driving epithelial-mesenchymal transition (EMT) via activation of the Notch signaling pathway.","authors":"Yuanyuan Wang, Jiquan Wen, Tingting Zhu, Xiangming Zha, Chengcheng Fang, Zhen Li, Lijun Shen, Tingjun Xu","doi":"10.1016/j.bbamcr.2026.120233","DOIUrl":"https://doi.org/10.1016/j.bbamcr.2026.120233","url":null,"abstract":"<p><p>Diabetic cataracts (DCs) are a major vision-threatening complication of diabetes mellitus; however, their molecular mechanisms remain incompletely understood. The present study aimed to investigate the role of the Notch ligand δ-like ligand 1 (DLL1) in the pathogenesis of DCs. Immunohistochemical analysis revealed elevated DLL1 expression in anterior lens capsule tissues from patients with DCs compared with patients with age-related cataracts. In vitro, high-glucose treatment combined with TGF-β2 treatment induced epithelial-mesenchymal transition (EMT) in human lens epithelial cells (HLEB3), and this was accompanied by increased DLL1 expression. Knockdown of DLL1 significantly suppressed TGF-β2-induced cell proliferation, migration and EMT, as evidenced by restored E-cadherin levels and reduced fibronectin and vimentin levels. Furthermore, the effects of DLL1 knockdown were enhanced by pharmacological inhibition of Notch signaling using N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT), confirming that DLL1 exerted its effects via the Notch pathway. In a streptozotocin-induced diabetic rat model, intravitreal administration of DLL1 small interfering RNA markedly attenuated lens opacity progression, improved lens histo-architecture, and downregulated the expression levels of EMT markers and Notch downstream targets (hes family bHLH transcription factor 1 and hes related family bHLH transcription factor with YRPW motif 1). Collectively, these findings demonstrated that DLL1 promoted DC progression by driving EMT via activation of the Notch signaling pathway. Therefore, targeting DLL1-mediated Notch signaling may potentially play a role in delaying or preventing DCs, although further studies are needed.</p>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":" ","pages":"120233"},"PeriodicalIF":4.3,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149147654","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

TMEM132A affects proliferation, invasion, and apoptosis via the β-catenin-dependent Wnt signaling in breast cancer TMEM132A通过β-catenin依赖的Wnt信号通路影响乳腺癌的增殖、侵袭和凋亡。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-06-01 Epub Date: 2026-05-26 DOI: 10.1016/j.bbamcr.2026.120162

Xiaoqiang Liu, Linmiao Qin, Huawei Yang

{"title":"TMEM132A affects proliferation, invasion, and apoptosis via the β-catenin-dependent Wnt signaling in breast cancer","authors":"Xiaoqiang Liu, Linmiao Qin, Huawei Yang","doi":"10.1016/j.bbamcr.2026.120162","DOIUrl":"10.1016/j.bbamcr.2026.120162","url":null,"abstract":"<div><div>Breast cancer continues to pose a significant health threat to women globally, highlighting the urgent need for novel therapeutic targets. The Wnt/β-catenin pathway plays an important role in tissue homeostasis. The Wnt/β-catenin signaling pathway frequently contributes to serious diseases, particularly cancer, through its dysregulation [1]. Transmembrane protein 132A (TMEM132A) serves as a potential regulator of the canonical Wnt pathway and is related to cancer progression. Nevertheless, the function of TMEM132A in breast cancer remains inadequately verified (Gao et al., 2023) [2]. In the present work, we initially confirmed the substantial overexpression of TMEM132A in breast cancer by analyzing TCGA, GEO, and GTEx datasets. This finding was further validated in breast cancer cell lines, where its expression correlated with unfavorable prognosis. TMEM132A overexpression was found to augment proliferation, migration, and invasion, and inhibit apoptosis in breast cancer cell lines (MDA-MB-231 and MCF-7), as demonstrated through functional validation, while its knockdown induced opposite effects. Mechanistically, TMEM132A knockdown reduced the expression of key Wnt pathway components, including Wnt3a, β-catenin, c-Myc, and Cyclin D1. Notably, nuclear and cytoplasmic fractionation assays demonstrated that TMEM132A promotes the nuclear accumulation of β-catenin, indicating enhanced activation of Wnt/β-catenin signaling. Furthermore, treatment with the Wnt inhibitor C59 attenuated the tumor-promoting effects induced by TMEM132A overexpression. Our findings establish that TMEM132A is a critical regulator of this signaling axis in cancer progression, highlighting its potential as a therapeutic target for breast cancer.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 5","pages":"Article 120162"},"PeriodicalIF":3.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148041002","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

Corrigendum to “Thermotolerance induced at a mild temperature of 40 °C alleviates heat shock-induced ER stress and apoptosis in HeLa cells” [Biochim. Biophys. Acta – Mol. Cell Res. 1853 (2015) 52–62/PMID: 25260982] “在40°C的温和温度下诱导的耐热性减轻热休克诱导的内质网应激和HeLa细胞凋亡”的勘误[biochem]。Biophys。分子细胞学报，1853 (2015)52-62/PMID: 25260982。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-06-01 Epub Date: 2026-04-30 DOI: 10.1016/j.bbamcr.2026.120150

Ahmed Bettaieb, Diana A. Averill-Bates

引用次数: 0

USP8/GPX4-based live-cell quantitative FRET imaging for ferroptosis drug screening 基于USP8/ gpx4的活细胞定量FRET成像用于铁下垂药物筛选。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-06-01 Epub Date: 2026-05-14 DOI: 10.1016/j.bbamcr.2026.120159

Xinghong Cai , Ziru Wu , Zhiyu Xiao , Guiping Zhuang , Zhengfei Zhuang

{"title":"USP8/GPX4-based live-cell quantitative FRET imaging for ferroptosis drug screening","authors":"Xinghong Cai , Ziru Wu , Zhiyu Xiao , Guiping Zhuang , Zhengfei Zhuang","doi":"10.1016/j.bbamcr.2026.120159","DOIUrl":"10.1016/j.bbamcr.2026.120159","url":null,"abstract":"<div><div>Targeting the functional interface between USP8 and GPX4 to disrupt ferroptosis defense represents a novel therapeutic strategy in cancer. Currently, there is a lack of drug screening models targeting the USP8/GPX4 interaction. This study utilized human breast cancer cell lines as a research model and established a drug screening platform capable of real-time, quantitative detection of USP8/GPX4 interactions in live cells based on fluorescence resonance energy transfer (FRET) imaging technology. We first confirmed that USP8 promotes malignant growth in breast cancer cells. Using the USP8 inhibitor DUB-IN-2 as a positive control alongside key ferroptosis markers, we employed FRET technology to quantitatively assess the interaction efficiency (<em>E</em><sub>D</sub>) between USP8 and GPX4. Screening of candidate compounds revealed that treatment with ML162, RSL3, and sorafenib resulted in maximum FRET efficiencies (<em>E</em><sub><em>Dmax</em></sub>) of 0.492, 0.483, and 0.503, respectively—significantly lower than that of control cells (0.548)—indicating effective disruption of USP8/GPX4 binding. This study successfully establishes a novel and efficient FRET-based drug screening model for targeting ferroptosis.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 5","pages":"Article 120159"},"PeriodicalIF":3.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147947209","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

USP1 represses ferroptosis in endometrial carcinoma cells by regulating the ubiquitination and stability of ESR1 USP1通过调控ESR1的泛素化和稳定性，抑制子宫内膜癌细胞的铁下垂。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-06-01 Epub Date: 2026-05-20 DOI: 10.1016/j.bbamcr.2026.120160

Qiaoyan Lin , Yanping Xiao , Jiuyue Liu , Rong Lu , Yujuan Chen , Jieyu Li , Xianren Ye

{"title":"USP1 represses ferroptosis in endometrial carcinoma cells by regulating the ubiquitination and stability of ESR1","authors":"Qiaoyan Lin , Yanping Xiao , Jiuyue Liu , Rong Lu , Yujuan Chen , Jieyu Li , Xianren Ye","doi":"10.1016/j.bbamcr.2026.120160","DOIUrl":"10.1016/j.bbamcr.2026.120160","url":null,"abstract":"<div><div>Endometrial carcinoma (EC) is a prevalent gynecologic malignancy. Ferroptosis, a type of programmed cell death, holds promise as a therapeutic strategy for cancer treatment. However, the specific role of ferroptosis and the underlying mechanisms in EC cells remain largely unexplored. In this study, we identified ubiquitin-specific protease 1 (USP1) as a key inhibitor of ferroptosis in EC cells. Our findings show that USP1 expression is reduced in EC cells undergoing ferroptosis but is elevated in EC tissues. Overexpressing USP1 significantly enhanced cell viability, colony formation, cell cycle progression, and migration/invasion capabilities, while strongly suppressing ferroptosis induced by the ferroptosis activator erastin. Through bioinformatic analysis and functional validation, we identified estrogen receptor 1 (ESR1) as a USP1-interacting protein involved in ferroptosis regulation. USP1 was shown to interact with ESR1, reduce its polyubiquitination, and enhance its protein stability. Rescue experiments revealed that ESR1 overexpression counteracted the pro-ferroptotic effects of USP1 depletion in erastin-treated EC cells. Finally, in vivo studies using an EC xenograft model confirmed the anti-ferroptotic and tumor-promoting role of the USP1-ESR1 axis. Together, our findings reveal a novel mechanism by which USP1 promotes EC progression through suppression of ferroptosis via ESR1 stabilization. Thus, targeting the USP1-ESR1 signaling axis may offer a new therapeutic strategy for EC.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 5","pages":"Article 120160"},"PeriodicalIF":3.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147970050","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 yin and yang interplay between HDAC6 and KDM1 regulates the lysosomal degradation of mutp53 in colon cancer cells undergoing TG-induced ER stress HDAC6和KDM1之间的阴阳相互作用调节tg诱导内质网络应激的结肠癌细胞中mutp53的溶酶体降解。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-06-01 Epub Date: 2026-05-26 DOI: 10.1016/j.bbamcr.2026.120164

Rossella Benedetti , Rosanna Paola Amato , Michele Di Crosta , Maria Saveria Gilardini Montani , Roberta Santarelli , Roberta Gonnella , Gabriella D'Orazi , Mara Cirone

{"title":"The yin and yang interplay between HDAC6 and KDM1 regulates the lysosomal degradation of mutp53 in colon cancer cells undergoing TG-induced ER stress","authors":"Rossella Benedetti , Rosanna Paola Amato , Michele Di Crosta , Maria Saveria Gilardini Montani , Roberta Santarelli , Roberta Gonnella , Gabriella D'Orazi , Mara Cirone","doi":"10.1016/j.bbamcr.2026.120164","DOIUrl":"10.1016/j.bbamcr.2026.120164","url":null,"abstract":"<div><div>Post-translational modifications (PTMs) play a key role in regulating protein/protein interactions and protein stability, thus influencing protein expression and function. HSPs and p53, including its wtp53 and mutp53 forms, make no exception to this rule, although the impact of PTMs on the regulation of these proteins has not yet been fully elucidated, particularly in the case of mutp53. These proteins, unlike wtp53, can behave as oncogenes, making their targeting an important step for successful anticancer therapy. We previously reported that mutp53 is degraded, preferentially via CMA, in colon cancer cells stressed by long-term TG treatment. Whether TG could induce PTMs and how they could contribute to mutp53 degradation has not yet been investigated and will be explored in this study. Acetylation of mutp53, as well as HSP90, has been reported to promote mutp53 degradation. However, we found that TG promoted deacetylation of mutp53 and HSP90, due to the sustained activity of HDAC6, a PTM that protected mutp53 from degradation. We then found that mutp53 was progressively demethylated by KDM1 at lysine K370 during TG treatment, which facilitated the interaction with HSC70 involved in mutp53 protein degradation via CMA. In conclusion, this study suggests that, in colon cancer cells subjected to stress by TG, mutp53 was degraded as a consequence of demethylation at lysine K370. Therefore, specific epigenetic drugs capable of reducing constitutive methylation and/or increasing acetylation could preemptively target mutp53 and improve the outcome of endoplasmic reticulum stress-inducing treatments in tumors harboring these proteins.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 5","pages":"Article 120164"},"PeriodicalIF":3.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148040968","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

Corrigendum to “Frequent EPHA2 receptor mutations in cholangiocarcinoma disrupt receptor forward signaling supporting a tumor suppressor role” [BBA Mol. Cell Res. 1873 (2026) 120081] “胆管癌中频繁的EPHA2受体突变破坏支持肿瘤抑制作用的受体前向信号传导”的更正[BBA Mol细胞杂志，1873(2026)120081]。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-06-01 Epub Date: 2026-03-20 DOI: 10.1016/j.bbamcr.2026.120139

Evodie Koutouan , Alejandro Lillo , Ayano Kabashima , Jack W. Sample , Danielle Carlson , Rondell Graham , Rory L. Smoot , Elena B. Pasquale

引用次数: 0

Corrigendum to “Involvement of mitochondrial and death receptor pathways in tributyltin-induced apoptosis in rat hepatocytes” [Biochim. Biophys. Acta 1693 (2004) 15–27 (15276321)] “线粒体和死亡受体通路在三丁基锡诱导的大鼠肝细胞凋亡中的参与”[生物化学]的更正。Biophys。Acta 1693(2004) 15-27(15276321)]。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-06-01 Epub Date: 2026-04-25 DOI: 10.1016/j.bbamcr.2026.120149

M. Jurkiewicz, D.A. Averill-Bates, M. Marion, F. Denizeau

引用次数: 0