Acta biochimica et biophysica Sinica最新文献_第2页

STC2 promotes cisplatin resistance through metabolic reprogramming and lactylation-mediated epigenetic regulation in cervical cancer. STC2在宫颈癌中通过代谢重编程和乳酸化介导的表观遗传调控促进顺铂耐药。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-29 DOI: 10.3724/abbs.2026169

Shanshan Jin, Dongqin Gao, Yaling Xiahou, Junxia Tao, Danna Jia, Lijuan Huang, Zhizhen Liu, Shulin Hou, Jun Xie, Huimin Lv

{"title":"STC2 promotes cisplatin resistance through metabolic reprogramming and lactylation-mediated epigenetic regulation in cervical cancer.","authors":"Shanshan Jin, Dongqin Gao, Yaling Xiahou, Junxia Tao, Danna Jia, Lijuan Huang, Zhizhen Liu, Shulin Hou, Jun Xie, Huimin Lv","doi":"10.3724/abbs.2026169","DOIUrl":"https://doi.org/10.3724/abbs.2026169","url":null,"abstract":"Cervical cancer (CC) is a major threat to women's health globally, and the development of cisplatin (DDP) resistance is a key factor leading to treatment failure. Prior research from our group has demonstrated the significant involvement of stanniocalcin-2 (STC2) in mediating DDP-resistance in CC. This study explores the role of STC2 in promoting chemoresistance through metabolic and epigenetic reprogramming. We find that STC2 is significantly upregulated in SiHa/DDP cells, a DDP-resistant subline of SiHa, where it enhances the malignant phenotype and drives glycolytic metabolism, increasing lactate production. The accumulated lactate subsequently elevates global histone lactylation, notably at the H3K18la site. Integrated CUT&Tag and RNA-seq analyses identify RBM20 as a potential downstream target of H3K18la-mediated transcriptional activation. Knockdown of STC2 reverses these effects, promoting chemosensitivity to DDP. Our results unveil a novel STC2/glycolysis/lactylation/RBM20 axis underlying DDP resistance in CC, providing new insights into potential therapeutic strategies to overcome chemoresistance by targeting this pathway.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079348","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

TET3 downregulation induces circadian disruption of BMAL1 through its DNA methylation-mediated repression in Alzheimer's disease. TET3下调通过DNA甲基化介导的阿尔茨海默病中BMAL1的抑制诱导其昼夜节律中断。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-25 DOI: 10.3724/abbs.2025189

Ting Liu, Jinxuan Fan, Jiangling Shi, Tian Mao, Xiuya Zhou, Kaili Du, Li Wang, Xiaohui Wang

{"title":"TET3 downregulation induces circadian disruption of BMAL1 through its DNA methylation-mediated repression in Alzheimer's disease.","authors":"Ting Liu, Jinxuan Fan, Jiangling Shi, Tian Mao, Xiuya Zhou, Kaili Du, Li Wang, Xiaohui Wang","doi":"10.3724/abbs.2025189","DOIUrl":"10.3724/abbs.2025189","url":null,"abstract":"Circadian disruptions appear at the presymptomatic stage of Alzheimer's disease (AD) and may exacerbate mental dysfunction in AD. The downregulation of brain and muscle ARNT-like protein 1 (BMAL1), a key clock element for the maintenance of circadian rhythms, has been linked to epigenetic mechanisms. Our previous study revealed that the mRNA level of DNA demethylase ten-eleven translocation ( Tet) 3 was reduced in the hippocampi of APPswe/PS1dE9 (APP/PS1) mice. However, the effects of TET3 on BMAL1 downregulation and circadian dysregulation in AD are still unclear. Our investigation first confirms that Tet3 mRNA and protein levels are decreased in both APP/PS1 mice and APPswe cells. In addition, decreased levels of 5hmC are observed in HT22 cells after TET3 knockdown, whereas TET3 overexpression reverses the reduction in 5hmC. Critically, we report that TET3 knockdown remethylates the Bmal1 promoter, thus downregulating BMAL1 expression in HT22 cells. In contrast, TET3 overexpression could upregulate BMAL1 by decreasing its methylation level. These results indicate that reduced TET3 is responsible for BMAL1 downregulation through decreased TET3 demethylation. Additionally, TET3 knockdown could lead to circadian disruption of BMAL1 in U2OS cells, whereas overexpression of TET3 alleviates the dysregulated biological rhythm in Aβ-treated U2OS cells. Our data suggest that TET3 plays a vital role in modulating the circadian rhythm at the epigenetic level through DNA demethylation.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"2060-2069"},"PeriodicalIF":4.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145385836","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 endotoxemia in metabolic and neurodegenerative diseases. 代谢性内毒素血症与神经退行性疾病。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-25 DOI: 10.3724/abbs.2026130

Changshun Li, Wei Jiang, Mingfang Lu

{"title":"Metabolic endotoxemia in metabolic and neurodegenerative diseases.","authors":"Changshun Li, Wei Jiang, Mingfang Lu","doi":"10.3724/abbs.2026130","DOIUrl":"10.3724/abbs.2026130","url":null,"abstract":"Metabolic diseases, which include obesity, type 2 diabetes, atherosclerosis, and metabolic dysfunction-associated steatotic liver disease (MASLD), are significant global health challenges. Patients with these conditions frequently exhibit gut dysbiosis and compromised gut barrier integrity, which lead to excessive translocation of Gram-negative bacterial lipopolysaccharide (LPS or endotoxin) from the gut lumen into the systemic circulation. This results in chronically elevated systemic LPS levels, a condition termed \"metabolic endotoxemia\". Gut-derived LPS may stimulate inflammatory responses and oxidative stress when it translocates and is recognized by host Toll-like receptor 4 (TLR4) and caspase-4/-5/-11. Metabolic endotoxemia is a primary trigger for the low-grade inflammation that promotes the development of metabolic diseases. Emerging evidence also indicates that metabolic endotoxemia acts as a key driver in the pathogenesis of neurodegenerative disorders, such as Alzheimer's disease, by promoting chronic neuroinflammation. In this review, we discuss: (1) the molecular structure of LPS that determines its bioactivity and its recognition by host cells, (2) host regulation of its bioactivity, (3) its translocation from the gut lumen into the systemic circulation, and (4) how metabolic endotoxemia contributes to obesity, type 2 diabetes, atherosclerosis, MASLD, and Alzheimer's disease. We conclude by exploring potential interventions aimed at preventing or mitigating metabolic endotoxemia by promoting LPS degradation and inactivation.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"1915-1930"},"PeriodicalIF":4.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148583326","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

MLN4924 promotes the transcriptional activation of BTG2 via the ROS/EGR1-mediated signaling axis to suppress acute myeloid leukemia progression. MLN4924通过ROS/ egr1介导的信号轴促进BTG2的转录激活，抑制急性髓系白血病的进展。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-25 DOI: 10.3724/abbs.2025194

Xiao Tang, Jinli Jian, Yuancheng Guo, Shujuan An, Long Zhao, Bei Liu

{"title":"MLN4924 promotes the transcriptional activation of BTG2 via the ROS/EGR1-mediated signaling axis to suppress acute myeloid leukemia progression.","authors":"Xiao Tang, Jinli Jian, Yuancheng Guo, Shujuan An, Long Zhao, Bei Liu","doi":"10.3724/abbs.2025194","DOIUrl":"10.3724/abbs.2025194","url":null,"abstract":"Acute myeloid leukemia (AML) is a highly heterogeneous hematological malignancy characterized by a high relapse rate and a low survival rate. Although chemotherapy and allogeneic hematopoietic stem cell transplantation (allo-HSCT) have improved the prognosis for AML patients, the overall survival rate remains suboptimal. MLN4924 is a neddylation inhibitor and is considered a promising treatment approach for AML. However, the exact molecular mechanism remains elusive and requires further investigation. This study aims to investigate the molecular mechanisms of MLN4924 and novel molecular pathways in AML. RNA sequencing (RNA-seq) reveals that the transcription factor (TF) EGR1 serves as a core regulator of MLN4924 and is upregulated by MLN4924 in AML. Mechanistic studies demonstrate that MLN4924 induces apoptosis by generating reactive oxygen species (ROS) and facilitates the nuclear translocation of EGR1. This translocated EGR1 interacts with the promoter region of BTG2, promoting its transcription and inhibiting the progression of AML. Notably, the ROS generated by MLN4924 influences the expression of both EGR1 and BTG2 and establishes a positive feedback loop between EGR1 and ROS. In vivo, we confirm that MLN4924 reduces the leukemic burden in AML cell-derived xenograft models by increasing the expression of both EGR1 and BTG2. In conclusion, these findings suggest that MLN4924 exerts an anti-tumor effect on AML by inducing apoptosis through the ROS-EGR1-BTG2 signaling axis. Our research provides a novel theoretical basis for the clinical potential of MLN4924 in improving the treatment of AML patients, offers novel strategies for AML treatment, and thereby advances the implementation of precision medicine.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"2070-2085"},"PeriodicalIF":4.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145909927","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

Andrographolide suppresses triple-negative breast cancer proliferation through the p53/CDK1 axis: a multiscale analysis combining network pharmacology and machine learning. 穿心术内酯通过p53/CDK1轴抑制三阴性乳腺癌增殖：结合网络药理学和机器学习的多尺度分析

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-25 DOI: 10.3724/abbs.2025210

Xiaoyong Sun, Zhensheng Peng, Heng Luo, Xinping Li, Jinyi Wu, Junjie Peng, Xinhai Xiao, Xuan Zheng, Hao Xiao, Haijian Zhong, Liang Zhang, Hua Wang

{"title":"Andrographolide suppresses triple-negative breast cancer proliferation through the p53/CDK1 axis: a multiscale analysis combining network pharmacology and machine learning.","authors":"Xiaoyong Sun, Zhensheng Peng, Heng Luo, Xinping Li, Jinyi Wu, Junjie Peng, Xinhai Xiao, Xuan Zheng, Hao Xiao, Haijian Zhong, Liang Zhang, Hua Wang","doi":"10.3724/abbs.2025210","DOIUrl":"10.3724/abbs.2025210","url":null,"abstract":"Triple-negative breast cancer (TNBC), a highly aggressive molecular subtype characterized by a lack of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) expression, remains a major clinical challenge, with a median overall survival of approximately 12-15 months in advanced-stage patients. Andrographolide (AG), a diterpenoid phytochemical derived from Andrographis paniculata, has demonstrated promising anti-inflammatory, antioxidant, and antitumor activities. However, its precise molecular and therapeutic mechanisms in TNBC remain poorly understood. AG inhibits the proliferation and metastasis of TNBC. Through an integrative approach combining network pharmacology and machine learning algorithms, including least absolute shrinkage and selection operator (LASSO) and random forest, cyclin-dependent kinase 1 (CDK1) has been identified as a critical molecular gene of AG. Experimental validation via western blot and immunofluorescence analyses reveal that AG treatment significantly downregulates CDK1 expression while concurrently upregulating the expression of the tumor suppressor p53, suggesting a functional interplay between these pathways. These mechanistic insights indicate that AG potentially exerts antiproliferative effects on TNBC cells through modulation of the p53/CDK1 signaling axis, thereby establishing a robust preclinical basis for its potential clinical translation in this challenging malignancy.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"2113-2124"},"PeriodicalIF":4.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145547747","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

Tolerogenic dendritic cells induced by withdrawal of polyunsaturated fatty acid DHA and mTOR inhibitor PP242 attenuate allograft rejection. 停用多不饱和脂肪酸DHA和mTOR抑制剂PP242诱导的耐受性树突状细胞可减轻同种异体移植排斥反应。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-25 DOI: 10.3724/abbs.2025214

Ning Wang, Hong Tang, Zhonghan Wu, Haiyang Xie, Hai Zhu, Danjing Guo, Yangwei Xiang, Zhi Liang, Ruiqi Sun, Shusen Zheng, Weili Han, Ke Zhou

{"title":"Tolerogenic dendritic cells induced by withdrawal of polyunsaturated fatty acid DHA and mTOR inhibitor PP242 attenuate allograft rejection.","authors":"Ning Wang, Hong Tang, Zhonghan Wu, Haiyang Xie, Hai Zhu, Danjing Guo, Yangwei Xiang, Zhi Liang, Ruiqi Sun, Shusen Zheng, Weili Han, Ke Zhou","doi":"10.3724/abbs.2025214","DOIUrl":"10.3724/abbs.2025214","url":null,"abstract":"Dendritic cells (DCs) exhibit the capacity to elicit either immune activation or tolerance, contingent upon diverse induction conditions. However, the crucial factors governing the induction of tolerogenic dendritic cells (Tol-DCs) remain obscure. Our study demonstrates that the combined use of docosahexaenoic acid (DHA) and the mammalian target of rapamycin inhibitor PP242 (comb-DHA) markedly hinders DC maturation while maintaining DC phagocytic capabilities in an immature state, thereby enabling substantial and sustained DHA accumulation within cells. Upon withdrawal of exogenous drug intervention, we observe that the retained DHA within the DCs facilitates delayed activation of p-AKT Ser473 and PTDSS2-related pathways, ultimately leading to the induction of a novel type of Tol-DC, comb-DHA-DC. These Tol-DCs display significantly reduced expression of costimulatory molecules and possess the ability to profoundly inhibit T-cell proliferation. Adoptive transfer of comb-DHA-DCs suppresses allograft rejection reactions. In summary, our findings reveal a novel strategy for inducing Tol-DCs and present a promising therapeutic avenue for enhancing graft tolerance.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"2102-2112"},"PeriodicalIF":4.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147300797","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

OAZ1/ CASP8AP2 double knockout enhances recombinant protein production in HEK293 cells through metabolic reprogramming and antiapoptotic effects. OAZ1/ CASP8AP2双敲除通过代谢重编程和抗凋亡作用增强HEK293细胞重组蛋白的产生。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-25 DOI: 10.3724/abbs.2025196

Junhe Zhang, Liao Zhang, Lu Hou, Weidong Li, Shaolei Geng, Xiaoyin Wang, Tianyun Wang

{"title":"OAZ1/ CASP8AP2 double knockout enhances recombinant protein production in HEK293 cells through metabolic reprogramming and antiapoptotic effects.","authors":"Junhe Zhang, Liao Zhang, Lu Hou, Weidong Li, Shaolei Geng, Xiaoyin Wang, Tianyun Wang","doi":"10.3724/abbs.2025196","DOIUrl":"10.3724/abbs.2025196","url":null,"abstract":"Human embryonic kidney (HEK) 293 cells are widely used for recombinant protein production because of their efficient posttranslational modification capabilities. However, their large-scale culture is often limited by metabolic stress and early apoptosis, leading to insufficient protein yields. In this study, we aim to increase protein expression through the coordinated modulation of metabolic and apoptotic pathways. Using CRISPR/Cas9 technology, we target and knockout the genes of ornithine decarboxylase antizyme 1 (OAZ1), which regulates polyamine metabolism, and caspase 8-associated protein 2 (CASP8AP2), an apoptosis-related protein. We successfully construct an OAZ1/ CASP8AP2 double-knockout HEK293 cell line. Following transfection with the knockout vector and screening of single-cell clones, multiple levels of validation confirm the successful gene knockout. The results show that the double-knockout cells exhibit significantly reduced apoptosis rates. Furthermore, the production of recombinant secreted alkaline phosphatase (SEAP) and vitronectin (VN) increases by 2.1 folds and 2.9 folds, respectively, compared with those in wild-type cells. Metabolic profiling reveals that the cell cycle is arrested in the G1/G0 phase, accompanied by increased specific consumption and production rates of key metabolites. This study demonstrates that concurrent inhibition of apoptosis and optimization of metabolism effectively enhances recombinant protein production in HEK293 cells, suggesting a novel strategy for improving HEK293 cell-based expression.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"2033-2043"},"PeriodicalIF":4.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146058288","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

Transcriptional regulation of GPSM2 by ZNF263 in colorectal cancer: implications for tumor aggressiveness. ZNF263在结直肠癌中GPSM2的转录调控：对肿瘤侵袭性的影响

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-25 DOI: 10.3724/abbs.2025181

Youquan Shi, Shantanu Baral, Youlei Zhang, Yongjun Jiang, Ruiqi Li, Yue Zhang, Wei Wang, Daorong Wang

{"title":"Transcriptional regulation of GPSM2 by ZNF263 in colorectal cancer: implications for tumor aggressiveness.","authors":"Youquan Shi, Shantanu Baral, Youlei Zhang, Yongjun Jiang, Ruiqi Li, Yue Zhang, Wei Wang, Daorong Wang","doi":"10.3724/abbs.2025181","DOIUrl":"10.3724/abbs.2025181","url":null,"abstract":"Colorectal cancer (CRC) is one of the most prevalent and lethal cancers worldwide and is characterized by uncontrolled cell invasion, migration, and proliferation. The progression of CRC is driven by genetic mutations and alterations in key signaling pathways. This study investigates the role of GPSM2 and ZNF263 implicated in CRC progression. The GPSM2 gene, which regulates G protein signaling pathways, plays a vital role in cell movement and growth, contributing to the metastatic potential of cancer cells. The ZNF263 gene, a zinc finger protein involved in gene expression regulation, is also linked to CRC progression, with its dysregulation affecting the cell cycle, apoptosis, and migration. In particular, this study explores how ZNF263 acts as a transcription factor, modulating the expression of GPSM2 to increase CRC cell invasion, migration, and proliferation. This study confirms that ZNF263 activates the cell cycle pathway in a GPSM2-dependent manner, driving the aggressive behavior of CRC cells. Bioinformatics analysis using the GEO database further supports these findings, identifying key genetic alterations in CRC. These insights provide a deeper understanding of the molecular mechanisms underlying CRC progression and highlight the potential of ZNF263 and GPSM2 as therapeutic targets for intervention. This study underscores the importance of early detection and exploration of targeted therapies to improve CRC patient outcomes.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"2044-2059"},"PeriodicalIF":4.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343185","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

SENP3 regulates DNA damage repair by downregulating RAP80 SUMOylation. SENP3通过下调RAP80 SUMOylation调节DNA损伤修复。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-25 DOI: 10.3724/abbs.2026075

Jianfeng Fu, Min Wei, Ruidan Xu, Xiaofeng Zheng

{"title":"SENP3 regulates DNA damage repair by downregulating RAP80 SUMOylation.","authors":"Jianfeng Fu, Min Wei, Ruidan Xu, Xiaofeng Zheng","doi":"10.3724/abbs.2026075","DOIUrl":"10.3724/abbs.2026075","url":null,"abstract":"Receptor-associated protein 80 (RAP80) is a key component of the BRCA1-A complex and plays an essential role in recruiting this complex to DNA double strand break (DSB) sites to facilitate homologous recombination (HR) repair. The function of RAP80 in DNA damage repair is tightly regulated by post-translational modifications (PTMs). However, the detailed mechanisms by which PTMs modulate RAP80 activity remain to be fully elucidated. Here, we demonstrate that SENP3 dynamically regulates DSB repair by targeting RAP80. Mechanistically, upon DNA damage, RAP80 undergoes SUMOylation and is recruited to DSB sites, promoting subsequent BRCA1 recruitment. SENP3 may facilitate the timely dissociation of RAP80 from DNA damage sites during the later stage, thereby promoting proper repair progression and ensuring timely termination of the DNA damage response. Dysregulation of RAP80 SUMOylation due to SENP3 depletion impairs HR repair and increases cellular sensitivity to irradiation and chemotherapy drugs. Collectively, our findings identify SENP3 as a key regulator of DNA repair through its dynamic control of RAP80-BRCA1 complex formation and DNA damage repair processes.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":"1949-1960"},"PeriodicalIF":4.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832208","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: PTBP1 promotes IRES-mediated translation of cyclin B1 in cancer. “PTBP1促进ires介导的肿瘤细胞周期蛋白B1的翻译”的更正。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-09-25 DOI: 10.3724/abbs.2025248

Xinyi Fan, Zitong Zhao, Liying Ma, Xuanlin Huang, Qimin Zhan, Yongmei Song

引用次数: 0