Acta biochimica et biophysica Sinica最新文献

5'-tiRNA-Lys maintains intestinal epithelial homeostasis by EWSR1-dependent suppression of miR-125a and autophagy activation. 5'-tiRNA-Lys通过依赖ewsr1抑制miR-125a和自噬激活来维持肠上皮稳态。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-06-23 DOI: 10.3724/abbs.2025074

Ningqin Xu, Ju Huang, Yiming Wang, Yaxin Liu, Yangwei Jiang, Wei Zhou, Jinghao Sheng, Lahong Zhang

{"title":"5'-tiRNA-Lys maintains intestinal epithelial homeostasis by EWSR1-dependent suppression of miR-125a and autophagy activation.","authors":"Ningqin Xu, Ju Huang, Yiming Wang, Yaxin Liu, Yangwei Jiang, Wei Zhou, Jinghao Sheng, Lahong Zhang","doi":"10.3724/abbs.2025074","DOIUrl":"10.3724/abbs.2025074","url":null,"abstract":"The intestinal epithelium relies on autophagy to maintain barrier integrity and homeostasis, and dysregulation of this process has been implicated in inflammatory bowel disease (IBD). While tRNA-derived small RNAs (tsRNAs) are emerging as regulators of cellular stress responses, their roles in intestinal autophagy remain poorly understood. Here, we identify that 5'-tiRNA-Lys, a tsRNA derived from mature tRNA-Lys, is significantly upregulated in the inflamed intestinal epithelium of IBD patients. Overexpression of 5'-tiRNA-Lys in mice ameliorates dextran sulfate sodium (DSS)-induced colitis. Mechanistically, 5'-tiRNA-Lys enhances autophagy in intestinal epithelial cells (IECs), as evidenced by elevated LC3-II level and autophagosome formation. RNA pull-down and immunoprecipitation assays reveal that 5'-tiRNA-Lys directly binds to the RNA-binding protein EWSR1 via its RNA recognition motif, disrupting EWSR1's interaction with the Drosha/DGCR8 microprocessor complex. This interference specifically suppresses the maturation of miR-125a, a microRNA that targets the autophagy-promoting gene UVRAG. Consequently, 5'-tiRNA-Lys increases UVRAG expression, thereby enhancing autophagic activity. Our findings reveal that 5'-tiRNA-Lys modulates autophagy through EWSR1-mediated miR-125a processing, which in turn affects intestinal inflammation, highlighting the potential of 5'-tiRNA-Lys as a therapeutic target for IBD.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144339763","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

TRIM25 ubiquitinates and degrades p62/SQSTM1 to suppress autophagy. TRIM25泛素化并降解p62/SQSTM1抑制自噬。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-06-20 DOI: 10.3724/abbs.2025062

Xiang Qiu, Jin Ren, Yun Yang, Weikang Hu, Chengcheng Wang, Ronggui Hu, Chuanyin Li

引用次数: 0

Dexamethasone induces ferroptosis in MC3T3-E1 cells by promoting DNMT3a-mediated Sirt1 DNA hypermethylation in the context of steroid-induced osteonecrosis of the femoral head. 地塞米松通过促进dnmt3a介导的Sirt1 DNA超甲基化，在类固醇诱导股骨头骨坏死的情况下诱导MC3T3-E1细胞铁凋亡。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-06-20 DOI: 10.3724/abbs.2025096

Kun Xiao, Huixia Yang, Chen Wang, Qian Zhang, Runqiu Ma, Xue'er Li, Ning Ding, Guizhong Li, Yinju Hao, Yideng Jiang, Jianmian Sun, Yue'e Chai, Zhigang Bai, Shengchao Ma

{"title":"Dexamethasone induces ferroptosis in MC3T3-E1 cells by promoting DNMT3a-mediated Sirt1 DNA hypermethylation in the context of steroid-induced osteonecrosis of the femoral head.","authors":"Kun Xiao, Huixia Yang, Chen Wang, Qian Zhang, Runqiu Ma, Xue'er Li, Ning Ding, Guizhong Li, Yinju Hao, Yideng Jiang, Jianmian Sun, Yue'e Chai, Zhigang Bai, Shengchao Ma","doi":"10.3724/abbs.2025096","DOIUrl":"10.3724/abbs.2025096","url":null,"abstract":"Ferroptosis, a novel form of regulated necrosis, has drawn the attention of the scientific community. Nevertheless, few studies have focused on the impact of ferroptosis on MC3T3-E1 cells in the context of steroid-induced osteonecrosis of the femoral head (SONFH). In this study, we explore the relationship between the degree of ferroptosis induced by dexamethasone (Dex) and the expression of silent information regulatory protein 1 (Sirt1). The results indicate that the ferroptosis level induced by Dex is mediated by the downregulation of Sirt1. Overexpression of Sirt1 increases the levels of the ferroptosis-related proteins SLC7A11 and GPX4 in MC3T3-E1 cells following Dex exposure. Moreover, the effect of Dex on Sirt1 expression is regulated by hypermethylation of the Sirt1 promoter, which is catalyzed by DNA methyltransferase 3a (DNMT3a). In summary, this study reveals that Dex can trigger ferroptosis by promoting DNMT3a-mediated DNA methylation and downregulating Sirt1 expression. Our findings provide an additional new mechanism for Dex-induced ferroptosis in MC3T3-E1 cells.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332273","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

Triptonide facilitates autophagy-mediated apoptosis in esophageal squamous cell carcinoma by targeting the AMPK-mTOR-ULK1 axis. 雷公藤内酯通过靶向AMPK-mTOR-ULK1轴促进食管鳞状细胞癌自噬介导的细胞凋亡。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-06-20 DOI: 10.3724/abbs.2025056

Jiujun Ju, Nuo Xu, Bohan Li, Dan Shi, Jiahui Cai, Qiusheng Zheng, Lei Ye, Shaosen Zhang, Caixia Wang

{"title":"Triptonide facilitates autophagy-mediated apoptosis in esophageal squamous cell carcinoma by targeting the AMPK-mTOR-ULK1 axis.","authors":"Jiujun Ju, Nuo Xu, Bohan Li, Dan Shi, Jiahui Cai, Qiusheng Zheng, Lei Ye, Shaosen Zhang, Caixia Wang","doi":"10.3724/abbs.2025056","DOIUrl":"10.3724/abbs.2025056","url":null,"abstract":"Triptonide (TN) is a small-molecule compound initially derived from Tripterygium wilfordii Hook. f used in traditional Chinese medicine. However, its potential antitumor mechanisms are still far from adequately understood. The purpose of this research is to elucidate the antitumor and pharmacological effects of TN on esophageal squamous cell carcinoma (ESCC). Functional assays, such as CCK-8 and colony formation assays, are used to evaluate the effects of TN on KYSE450 and KYSE510 cells. Subsequently, western blot analysis, Hoechst 33258 staining, flow cytometric analysis, autophagic flux detection, and transmission electron microscopy (TEM) are used to determine the effects of TN on apoptosis and autophagy in ESCC cells. Additionally, the autophagy inhibitor 3-methyladenine (3-MA) and the AMPK inhibitor dorsomorphin (Compound C, CC) are administered to explore the molecular mechanisms and crucial pathways in ESCC cells. Our findings provide strong evidence that TN induces autophagy-dependent apoptosis by targeting the AMPK-mTOR-ULK1 axis in ESCC cells. Collectively, this study sheds light on the anticancer mechanisms of TN in esophageal squamous cell carcinoma and suggests that TN is a promising candidate for the antitumor phytomedicine.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144339799","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

FOXD3 promotes homologous recombination repair and genomic stability by facilitating MRE11-mediated DNA end resection. FOXD3通过促进mre11介导的DNA末端切除，促进同源重组修复和基因组稳定性。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-06-13 DOI: 10.3724/abbs.2025063

Shibin Xu, Jingyu Zhang, Congwen Gao, Ziyi Xiong, Yamin Gong, Bao Chai, Hongxiang Chen, Xingzhi Xu

引用次数: 0

Melatonin attenuates kidney injury by alleviating lysosomal damage in diabetic kidney disease. 褪黑素通过减轻糖尿病肾病的溶酶体损伤来减轻肾损伤。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-06-13 DOI: 10.3724/abbs.2025034

Jiaqi Chen, Shuting Zhang, Xiaoquan Xue, Xiaoqin Ma, Aomiao Chen, Yichuan Wu, Geningyue Wang, Qian Zhang, Yaoming Xue, Yijie Jia, Zongji Zheng

{"title":"Melatonin attenuates kidney injury by alleviating lysosomal damage in diabetic kidney disease.","authors":"Jiaqi Chen, Shuting Zhang, Xiaoquan Xue, Xiaoqin Ma, Aomiao Chen, Yichuan Wu, Geningyue Wang, Qian Zhang, Yaoming Xue, Yijie Jia, Zongji Zheng","doi":"10.3724/abbs.2025034","DOIUrl":"https://doi.org/10.3724/abbs.2025034","url":null,"abstract":"Proteinuria-induced damage to renal tubular epithelial cells is one of the main causes of diabetic kidney disease (DKD), and the clearance of overloaded albumin by lysosomes is crucial for maintaining the homeostasis of renal tubular epithelial cells. Therefore, lysosomal damage is closely related to the pathogenesis of DKD, but effective prevention and treatment measures are still lacking. Melatonin (MLT) is secreted by the pineal gland and can not only regulate circadian rhythms but also maintain lysosomal homeostasis. In this study, we demonstrate the presence of significant lysosomal damage in the renal tubules of DKD patients, which causes autophagy impairment and a concomitant oxidative stress imbalance; however, MLT can upregulate transcription factor EB (TFEB) to improve lysosomal damage and restore the biosynthesis of this organelle. Mechanistically, MLT may protect lysosomes via the upregulation of TFEB and the miR-205-5p‒LRP-1 pathway in renal tubules, thus improving autophagy dysfunction and oxidative imbalance in DKD.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144281950","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

HECTD3 is overexpressed in breast cancer and associated with a good prognosis. hector 3在乳腺癌中过表达，并与良好预后相关。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-06-13 DOI: 10.3724/abbs.2025073

Yingying Wu, Fubing Li, Hailin Zhang, Dingyun You, Yanjie Kong, Zhongmei Zhou, Songqing Fan, Ceshi Chen

引用次数: 0

Melatonin mitigates ovarian aging through regulation of the YTHDF2/m⁶A/UBE3C axis. 褪黑素通过调节YTHDF2/m6A/UBE3C轴来减缓卵巢衰老。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-06-11 DOI: 10.3724/abbs.2025090

Wenjuan Xia, Xin Wang, Jincheng Li, Ming Zhang, Jiafeng Lu, Hong Li, Quanze He, Qingxia Meng, Boxian Huang

{"title":"Melatonin mitigates ovarian aging through regulation of the YTHDF2/m6A/UBE3C axis.","authors":"Wenjuan Xia, Xin Wang, Jincheng Li, Ming Zhang, Jiafeng Lu, Hong Li, Quanze He, Qingxia Meng, Boxian Huang","doi":"10.3724/abbs.2025090","DOIUrl":"https://doi.org/10.3724/abbs.2025090","url":null,"abstract":"Ovarian aging is a natural process characterized by a decline in both the quantity and quality of oocytes, which subsequently leads to diminished fertility, particularly in women over the age of 35. Given the societal trend toward postponing childbirth, it is imperative to understand the molecular mechanisms that underpin ovarian aging to address infertility issues. Melatonin (MT) is recognized for its therapeutic potential in mitigating ovarian aging; however, the specific epigenetic mechanisms involved, particularly concerning m6A methylation, remain inadequately defined. Our investigation demonstrates that MT mitigates ovarian aging in murine models, significantly decreasing m6A methylation levels. <italic>In vitro</italic> analyses of ovarian granulosa (KGN) cells reveals a marked increase in YTHDF2 expression, with differentially methylated genes being notably enriched in the polyubiquitination pathway. Further examination shows that YTHDF2 enhances the expression of the E3 ligase UBE3C by modulating the m6A methylation of <italic>UBE3C</italic> mRNA, thereby reducing the expression of the P53 senescence factor and alleviating the effects of ovarian aging..","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265026","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

PDGFC secreted by cancer-associated fibroblasts promotes epithelial-mesenchymal transition and immunosuppression in lung adenocarcinoma. 肺癌相关成纤维细胞分泌PDGFC促进肺腺癌上皮-间质转化和免疫抑制。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-06-11 DOI: 10.3724/abbs.2025042

Meimei Cui, Xiaodi Ding, Yu Jiang, Liying Zhang, Wangkai Cao, Yongming Wang, Zhimei Sheng, Wei Sun, Ai Guo, Lihui Gu, Xiurong Zhang, Wanli Duan, Lihong Shi, Baogang Zhang

{"title":"PDGFC secreted by cancer-associated fibroblasts promotes epithelial-mesenchymal transition and immunosuppression in lung adenocarcinoma.","authors":"Meimei Cui, Xiaodi Ding, Yu Jiang, Liying Zhang, Wangkai Cao, Yongming Wang, Zhimei Sheng, Wei Sun, Ai Guo, Lihui Gu, Xiurong Zhang, Wanli Duan, Lihong Shi, Baogang Zhang","doi":"10.3724/abbs.2025042","DOIUrl":"https://doi.org/10.3724/abbs.2025042","url":null,"abstract":"This study elucidates the mechanisms by which cancer-associated fibroblast (CAF)-derived platelet-derived growth factor C (PDGFC) promotes the progression of lung adenocarcinoma (LUAD) and explores the impact of PDGFC on immune regulation within the tumor microenvironment (TME). Our results show that there is higher expression of PDGFC in CAFs than in nontumor tissue fibroblasts (NFs) and that higher expression of PDGFC is correlated with poor prognosis in LUAD patients. Furthermore, CAF-derived PDGFC promotes epithelial-mesenchymal transition (EMT) in cancer cells as well as matrix metalloproteinase 2 (MMP2) expression through the PDGF receptor A (PDGFRA)-mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway. Moreover, our study demonstrates that CAF-derived PDGFC is essential for the activation and infiltration of fibroblasts in the TME, as well as the inflammatory infiltration of different immune cell types and the immunosuppressive conditions within the TME. In particular, PDGFC induces increased PDGFRA expression in both tumor cells and fibroblasts, which can lead to reciprocally positive feedback to accelerate malignant tumor progression. This discovery provides a novel TME-targeted strategy for LUAD treatment.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273848","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

Gankyrin-deficiency reprograms intrahepatic glucose and lipid metabolism to delay liver regeneration. 肝精素缺乏症重编程肝内葡萄糖和脂质代谢，延缓肝脏再生。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-06-06 DOI: 10.3724/abbs.2025086

Yitian Liu, Yiwei Sun, Lv Jin, Ying Xu, Bibo Wang, Ting Yu, Xiaofei Wei, Jing Xu, Yating Wei, Shuai Yang, Min Yu, Hongyang Wang, Yao Chen

{"title":"Gankyrin-deficiency reprograms intrahepatic glucose and lipid metabolism to delay liver regeneration.","authors":"Yitian Liu, Yiwei Sun, Lv Jin, Ying Xu, Bibo Wang, Ting Yu, Xiaofei Wei, Jing Xu, Yating Wei, Shuai Yang, Min Yu, Hongyang Wang, Yao Chen","doi":"10.3724/abbs.2025086","DOIUrl":"https://doi.org/10.3724/abbs.2025086","url":null,"abstract":"Liver regeneration is a critical adaptive response to hepatic injury, requiring precise metabolic reprogramming to meet the energetic and biosynthetic demands of proliferating hepatocytes. While the oncoprotein Gankyrin is well-established as a promoter of liver fibrosis and hepatocarcinogenesis, its role in metabolic adaptations underlying liver regeneration remains unclear. In this study, we demonstrate that Gankyrin deficiency in the liver ( Gank △Hep/Y) induces hepatic hypertrophy and aberrant glycogen accumulation. Gankyrin expression is significantly upregulated after partial hepatectomy (PHx), whereas Gank △Hep/Y -PHx mice exhibit impaired liver regeneration. This impairment is marked by a delayed restoration of the liver-to-body weight ratio, blunted glycogenolysis, and reduced fatty acid uptake. Mechanistically, Gankyrin activates Pygl and Cd36, key regulators of glycogenolysis and lipid uptake, respectively. Pharmacological inhibition of PYGL activity retards liver regeneration. Furthermore, we identify a novel interaction between Gankyrin and FOXO1, wherein Gankyrin promotes FOXO1 ubiquitination and subsequent proteasomal degradation. This Gankyrin-dependent suppression of FOXO1 leads to the transcriptional upregulation of Pygl and Cd36, thereby fueling hepatocyte proliferation. Collectively, our findings reveal Gankyrin as a master regulator of liver regeneration, integrating metabolic reprogramming with proliferative signaling through the FOXO1-PYGL/CD36 axis. These insights not only elucidate the mechanistic underpinnings of liver regeneration but also unveil the therapeutic potential of targeting the Gankyrin/FOXO1 pathway to mitigate hepatic insufficiency and enhance regenerative capacity in clinical settings.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144232837","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