Molecular and Cellular Biology最新文献_第6页

KLF11 in Extracellular Vesicles Derived from adMSCs Inhibits Colorectal Cancer via Suppressing SOAT1-Mediated Lipogenesis. adMSCs细胞外囊泡中的KLF11通过抑制soat1介导的脂肪生成抑制结直肠癌。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2026-07-14 DOI: 10.1080/10985549.2026.2685572

Fan Yang, Haitao Yu, Jian Ni, Yuqing Sun, Xiaowen Zhu, Haidong Wang, Xingwang Zhao, Bin Zhao

{"title":"KLF11 in Extracellular Vesicles Derived from adMSCs Inhibits Colorectal Cancer via Suppressing SOAT1-Mediated Lipogenesis.","authors":"Fan Yang, Haitao Yu, Jian Ni, Yuqing Sun, Xiaowen Zhu, Haidong Wang, Xingwang Zhao, Bin Zhao","doi":"10.1080/10985549.2026.2685572","DOIUrl":"10.1080/10985549.2026.2685572","url":null,"abstract":"Colorectal cancer (CRC) remains one of the most frequently diagnosed and lethal malignancies. Recent studies showed that either adipose-derived mesenchymal stem cells (adMSCs) or the extracellular vesicles (EVs) they secrete retarded CRC progression. Here, we investigated the mechanism underlying the role of adMSCs-EVs in CRC. Here, we found that Krüppel-like factor 11 (KLF11) was upregulated in adMSCs-EVs. adMSCs-EVssh-KLF11 (EVs derived from KLF11-depleted adMSCs) effectively promoted lipogenesis, cell viability, proliferation, migration, and invasion of CRC cells, and accelerated tumor growth in mice. Furthermore, KLF11 carried by adMSCs-EVs dampened the PI3K/AKT signaling pathway by transcriptionally repressing sterol o-acyltransferase 1 (SOAT1) expression. SOAT1 knockdown blocked the enhanced lipogenesis, proliferation, migration and invasion induced by adMSCs-EVssh-KLF11. In conclusion, KLF11 derived from adMSCs-EVs inactivated the PI3K/AKT signaling pathway by transcriptionally downregulating SOAT1, therefore suppressing lipogenesis and malignant progression of CRC.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"909-926"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148437368","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

Transcription Factors in Breast Cancer Oncogenesis and Progression. 乳腺癌发生和发展中的转录因子。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2026-07-04 DOI: 10.1080/10985549.2026.2694520

Lianna Fiore, Zhijie Li, Collin Montgomery, Audrey Coleman, Colin Kenny, Ronald J Weigel

引用次数: 0

ZRANB1 and ACSS2 Cooperate to Regulate Ubiquitination and Acetylation to Stabilize TWIST1 in Breast Cancer Metastasis. ZRANB1和ACSS2协同调节泛素化和乙酰化以稳定TWIST1在乳腺癌转移中的作用

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2026-07-07 DOI: 10.1080/10985549.2026.2694523

Yeqing Xu, Liufang Zhou, Dizheng Liao, Miduo Tan, Jian Chen

{"title":"ZRANB1 and ACSS2 Cooperate to Regulate Ubiquitination and Acetylation to Stabilize TWIST1 in Breast Cancer Metastasis.","authors":"Yeqing Xu, Liufang Zhou, Dizheng Liao, Miduo Tan, Jian Chen","doi":"10.1080/10985549.2026.2694523","DOIUrl":"10.1080/10985549.2026.2694523","url":null,"abstract":"The epithelial-mesenchymal transition (EMT) transcription factor TWIST1 plays a critical role in breast cancer progression. This study reveals that TWIST1 acetylation, which is elevated in metastatic breast cancer tissues, is regulated by a deubiquitination-acetylation crosstalk. We demonstrate that ZRANB1 binds to and deubiquitinates TWIST1, thereby increasing its protein stability. This stabilization enhances the interaction between TWIST1 and the acetyltransferase ACSS2, leading to further TWIST1 acetylation. ACSS2 overexpression reversed ZRANB1 knockdown-induced inhibition of TWIST1 acetylation. Functionally, ZRANB1 overexpression promoted breast cancer cell proliferation, invasion, migration, and EMT in vitro, as well as lung metastasis in vivo, all of which were reversed by ACSS2 knockdown. Conversely, ACSS2 knockdown suppressed TWIST1 acetylation, EMT, and metastatic capabilities. Consistently, ACSS2 overexpression rescued the inhibitory effects of ZRANB1 knockdown on breast cancer cell viability, proliferation, migration, and invasion. In summary, our findings identify a novel regulatory axis wherein ZRANB1-mediated deubiquitination facilitates ACSS2-dependent acetylation to stabilize TWIST1, thereby driving EMT and metastasis in breast cancer. The ZRANB1/ACSS2 axis presents a promising therapeutic target for combating metastasis.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"927-947"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148397367","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

Cholesterol Transport from ER to Outer Mitochondria by ERLIN2 in Steroid Metabolism. 类固醇代谢中ERLIN2介导胆固醇从内质网转运至外线粒体。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2025-11-18 DOI: 10.1080/10985549.2025.2583172

Himangshu S Bose, William E Burak, Randy M Whittal

引用次数: 0

Impact of Transposable Elements on DNA Double-Strand Break Repair and Genomic Stability. 转座因子对DNA双链断裂修复和基因组稳定性的影响。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2026-01-11 DOI: 10.1080/10985549.2025.2594182

Mohd Iqbal Bhat, Raj K Pandita, Arjamand Mushtaq, Ulfat S Mir, Najumu Saqib, Partha S Sarkar, Audesh Bhat, Kenneth S Ramos, Tej K Pandita, Mohammad Altaf

引用次数: 0

Chaihu Shugan Powder Attenuates Ferroptosis-Associated Injury in Acute Pancreatitis by Activating PGC-1α/Nrf2/HO-1 Pathway. 柴胡疏肝散通过激活PGC-1α/Nrf2/HO-1通路减轻急性胰腺炎铁中毒相关损伤

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2026-03-16 DOI: 10.1080/10985549.2026.2638200

Yutao Chen, Dapeng Zhang, Quan Li, Yingqing Xing

{"title":"Chaihu Shugan Powder Attenuates Ferroptosis-Associated Injury in Acute Pancreatitis by Activating PGC-1α/Nrf2/HO-1 Pathway.","authors":"Yutao Chen, Dapeng Zhang, Quan Li, Yingqing Xing","doi":"10.1080/10985549.2026.2638200","DOIUrl":"10.1080/10985549.2026.2638200","url":null,"abstract":"Acute pancreatitis (AP) is a life-threatening condition driven by premature pancreatic enzyme activation, leading to systemic complications and multi-organ dysfunction. Chaihu Shugan Powder (CSP) has been reported to mitigate pancreatic injury associated with AP, but the detailed regulatory mechanism was unclear. In our study, we investigated the fundamental mechanism of how CSP attenuated AP injury. The AP models were constructed by applying cerulein in AR42J cells and rats. Individual CSP interventions did not affect normal cell function. CSP partially reversed cerulein-induced cell damage, as reflected by increased cell viability, the level of glutathione (GSH), and ferroptosis protein markers but decreased the contents of inflammatory factor, reactive oxygen species (ROS), malondialdehyde (MDA), Fe2+ and iron. CSP activated the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, which in turn reduced ferroptosis in cerulein-exposed AR42J cells. Silencing the PGC-1α gene could partially inhibit the activation of the PGC-1α/Nrf2/HO-1 pathway by CSP in cerulein-induced AR42J cells. In AP rats, CSP alleviated AP-related pathomorphological changes and ferroptosis in rats by activating PGC-1α/Nrf2/HO-1 pathway. Altogether, the mechanism by which CSP alleviated AP injury in rats may be correlated with the activation of PGC-1α/Nrf2/HO-1 pathway.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"641-654"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147468545","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

PUF60 is a Critical Regulator of PKM Splicing During Myogenesis. PUF60是肌发生过程中PKM剪接的关键调节因子。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2026-07-14 DOI: 10.1080/10985549.2026.2699151

So Masaki, Takayuki Nojima, Takako Oshiro-Ideue, Asami Suenaga, Akihide Takeuchi, Isao Kii, Kenji Suzuki, Satoshi Tanaka, Masatoshi Hagiwara, Naoyuki Kataoka

{"title":"PUF60 is a Critical Regulator of PKM Splicing During Myogenesis.","authors":"So Masaki, Takayuki Nojima, Takako Oshiro-Ideue, Asami Suenaga, Akihide Takeuchi, Isao Kii, Kenji Suzuki, Satoshi Tanaka, Masatoshi Hagiwara, Naoyuki Kataoka","doi":"10.1080/10985549.2026.2699151","DOIUrl":"10.1080/10985549.2026.2699151","url":null,"abstract":"Pyruvate kinase M (PKM) catalyzes the conversion of phosphoenolpyruvate to pyruvate in glycolysis and exists as two splice isoforms, PKM1 and PKM2, generated from alternative splicing of mutually exclusive exons 9 or 10, respectively. The expression balance between PKM1 and PKM2 is tightly regulated in a cell-type-specific manner. PKM1 is predominantly expressed in tissues such as skeletal muscle, heart, and brain, whereas PKM2 is prevalent in most other tissues and various cancer cells. Despite its importance, the trans-acting factors promoting exon 9 selection in a tissue-specific context remain largely unknown. Here, using a multi-color splicing reporter system for cell-based cDNA screening, we identified PUF60 as a novel trans-acting factor that promotes PKM1-type splicing. We also demonstrated that PUF60 induction and the resulting splicing switch are essential for myotube formation during C2C12 differentiation. This study establishes PUF60 as a critical regulator of muscle-specific splicing and provides new insights into the fundamental mechanisms governing skeletal muscle differentiation.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"970-985"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148437386","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

Qi Lian Jie Ning Ameliorates DSS-Induced Colitis in Rats by Inhibition of JAK2/STAT3 and TLR4/NF-kB Pathways. 芪连解宁通过抑制JAK2/STAT3和TLR4/NF-kB通路改善dss诱导大鼠结肠炎。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2025-11-25 DOI: 10.1080/10985549.2025.2580429

Jinyang Hu, Songlin Zeng, Shisheng Jiang, Yuhua Wu, Junjie Niu

{"title":"Qi Lian Jie Ning Ameliorates DSS-Induced Colitis in Rats by Inhibition of JAK2/STAT3 and TLR4/NF-kB Pathways.","authors":"Jinyang Hu, Songlin Zeng, Shisheng Jiang, Yuhua Wu, Junjie Niu","doi":"10.1080/10985549.2025.2580429","DOIUrl":"10.1080/10985549.2025.2580429","url":null,"abstract":"Ulcerative colitis (UC) is a clinically common idiopathic inflammatory bowel disease. The DSS-induced colitis model was induced via 5% DSS for 7 days. Rats were gavaged with QLJCN solution in different concentrations. This study measured body weight, colon length, and DAI of rats in each group. The hematoxylin-eosin staining assessed the histopathology and histological score. Western blot analysis examined the expressions of TFF3, MUC-2, JAK2/STAT3 pathway-, and TLR4/NF-κB pathway-related markers. Moreover, the contents of IL-6, TNF-α, and LPS in the colons/serum were determined by ELISA. TLR4 activator (RS09) or JAK2/STAT3 activator (colivelin) were employed for the rescue experiments. QLJCN repressed weight loss and the increase of DAI score in DSS rats. QLJCN also increased the colon length and alleviated colonic damage, and effectively repressed the levels of IL-6 and TNF-α but elevated the levels of TFF3 and MUC-2 in the colons/serum of DSS rats. Moreover, QLJCN weakened the activation of JAK2/STAT3 and TLR4/NF-κB pathways, and alleviated the intestinal inflammation. Furthermore, these ameliorative effects of QLJCN were reversed by TLR4 activator (RS09) or JAK2/STAT3 activator (colivelin). QLJCN has protective effects on DSS-induced colitis rats by restraining JAK2/STAT3 and TLR4/NF-κB pathways. This study provides new therapeutic strategies for UC.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"475-486"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145605029","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

Metabolic Regulation of Copper Homeostasis Governs the Sec61-Dependent Protein Translocation Process in Saccharomyces cerevisiae. 铜稳态的代谢调控调控了酿酒酵母中sec61依赖的蛋白易位过程。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2025-10-14 DOI: 10.1080/10985549.2025.2569577

Vandana Anjana, Smriti Anand, Prateeksha Thakur, Rajshree Pal, Santoshi Acharjee, Sugandh Sharma, Sharayu Subhash Awachat, Ritika Manjhi, Devika Rejidev, Ranu Singh, Raghuvir Singh Tomar

{"title":"Metabolic Regulation of Copper Homeostasis Governs the Sec61-Dependent Protein Translocation Process in Saccharomyces cerevisiae.","authors":"Vandana Anjana, Smriti Anand, Prateeksha Thakur, Rajshree Pal, Santoshi Acharjee, Sugandh Sharma, Sharayu Subhash Awachat, Ritika Manjhi, Devika Rejidev, Ranu Singh, Raghuvir Singh Tomar","doi":"10.1080/10985549.2025.2569577","DOIUrl":"10.1080/10985549.2025.2569577","url":null,"abstract":"The concentration of cellular labile pool of copper must be strictly regulated because disruption in copper homeostasis results in diseases. In Saccharomyces cerevisiae, elevated levels of labile copper impair cell viability by inhibiting Sec61-mediated protein translocation into the endoplasmic reticulum. We investigated how metabolic pathways, specifically mitochondrial respiration and autophagy, contribute to copper homeostasis and the translocation of secretory proteins. We show that copper selectively inhibits protein translocation in yeast cells grown in minimal medium but not in a rich medium, highlighting a critical role of nutrients in modulating copper toxicity. Supplementation of specific amino acids suppresses the copper-induced defects in protein translocation and cell death, identifying amino acids as suppressors of the copper toxicity. Using a panel of gene deletion mutants affecting mitochondrial functions, autophagy, peroxisomes, and lipid droplets, we demonstrate that metabolic pathways regulate subcellular concentration of copper and translocation of secretory proteins. Further, disruption of redox and pH homeostasis, and pharmacological inhibition of respiration, reveals that correct subcellular concentration of copper is essential to prevent inhibitory effects on protein translocation. Together, our findings provide mechanistic insights into how metabolic status influences cellular copper homeostasis and the secretory pathway of proteins, with broader implications for understanding diseases of copper metabolism.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"48-77"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145286437","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

p62 Coordinates Autophagy, cAMP Signalling, and Cell-Fate Determination in Dictyostelium discoideum. p62在盘状盘基骨柱中协调自噬、cAMP信号传导和细胞命运决定。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2026-02-22 DOI: 10.1080/10985549.2026.2627237

Saksham Gautam, Shweta Saran

{"title":"p62 Coordinates Autophagy, cAMP Signalling, and Cell-Fate Determination in Dictyostelium discoideum.","authors":"Saksham Gautam, Shweta Saran","doi":"10.1080/10985549.2026.2627237","DOIUrl":"10.1080/10985549.2026.2627237","url":null,"abstract":"p62/SQSTM1 is a multifunctional adaptor protein playing a central role in the regulation of autophagy and stress response pathways in higher eukaryotes. However, its functional relevance in lower eukaryotes like Dictyostelium remains largely unexplored. In this study, we demonstrate that Dictyostelium p62 is crucial for cAMP-mediated development and autophagy. Loss of p62 alters levels of intracellular glucose, cAMP, ubiquitinated proteins and autophagic flux. These defects result in impaired cell aggregation and abnormal fruiting body formation, accompanied by reduced spore viability. Interestingly, pulsing of p62 null cells with exogenous cAMP could partially rescue the developmental defects, implicating a role of p62 in maintaining the intracellular cAMP levels required for starvation stress-induced development. p62 also influences cell-fate decisions during development as its deletion biases cells toward pre-spore differentiation, whereas overexpression promotes pre-stalk lineage. Mechanistically, p62 also modulates autophagy flux potentially via regulating AMPK levels along with cAMP dynamics. Together, these findings position p62 as an evolutionarily conserved key adaptor protein that provides new insights into the molecular mechanisms underlying multicellular development.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"566-583"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147271369","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