Acta biochimica et biophysica Sinica最新文献_第6页

PGC7 maintains the pluripotency of F9 embryonic carcinoma cells by promoting Nanog translation. PGC7通过促进Nanog翻译维持F9胚胎癌细胞的多能性。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-12 DOI: 10.3724/abbs.2025035

Yingxiang Liu, Xing Wei, Caixia Zhang, Jingya Liu, Mengying Yu, Peiwen Feng, Zekun Guo

{"title":"PGC7 maintains the pluripotency of F9 embryonic carcinoma cells by promoting Nanog translation.","authors":"Yingxiang Liu, Xing Wei, Caixia Zhang, Jingya Liu, Mengying Yu, Peiwen Feng, Zekun Guo","doi":"10.3724/abbs.2025035","DOIUrl":"https://doi.org/10.3724/abbs.2025035","url":null,"abstract":"Primordial germ cell 7 (PGC7) is prominently expressed in primordial germ cells (PGCs) and embryonic stem cells (ESCs), serving as a pivotal marker for discerning stem cell pluripotency. However, the role of PGC7 in regulating core pluripotency factors remains unclear. In this study, the expression dynamics of PGC7 and pluripotency- associated proteins are systematically evaluated by quantitative reverse transcription PCR (RT-qPCR) and western blot analysis. Complementary experimental approaches including confocal immunofluorescence and Co- immunoprecipitation (Co-IP) assays are subsequently employed to establish subcellular colocalization patterns and elucidate the molecular mechanisms associated with PGC7 function. The results show that PGC7 is closely associated with the pluripotency status of F9 embryonal carcinoma (EC) cells. Notably, PGC7 can counteract the decrease in pluripotency induced by retinoic acid (RA). Ectopic expression of PGC7 in F9 EC cells enhances the translation of Nanog. Mechanistic analysis reveal that PGC7 activates Y-box binding protein 1 (YBX1) phosphorylation by enhancing the interaction between YBX1 and AKT1. The subsequent phosphorylation of YBX1 reduces its binding to Nanog mRNA and promotes the translation of Nanog. These results shed light on a previously unknown role of PGC7 in supporting the translation of Nanog, offering valuable insights into the functions of PGC7 in F9 EC cells.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603206","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

Sandwich-type graphene electrochemical sensor for nucleic acid detection of SARS-CoV-2. 新型冠状病毒核酸检测的三明治式石墨烯电化学传感器

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-12 DOI: 10.3724/abbs.2025015

Huan Yang, Yating Li, Donglin Cao, Li He, Yingjian Guo, Zhongming Liu, Haiyan Zhang

引用次数: 0

NCOA6 knockdown enhances RSL3-induced ferroptosis in pancreatic cancer cells and increases the sensitivity to gemcitabine. NCOA6敲低可增强rsl3诱导的胰腺癌细胞铁下垂，并增加对吉西他滨的敏感性。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-10 DOI: 10.3724/abbs.2024221

Yuming Jia, Zeng Ye, Xin Wang, Yanli Deng, Chao Wang, Zhilei Zhang, Guixiong Fan, Wuhan Yang, Xiaowu Xu, Yi Qin, Li Peng

引用次数: 0

HDAC11 in ovarian granulosa cells coordinates LH in the maturation of oocytes in Tan sheep. 滩羊卵巢颗粒细胞中的HDAC11在卵母细胞成熟过程中协调LH。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-10 DOI: 10.3724/abbs.2025036

Jiaqi Shi, Donghuan Lv, Yaxiu Xu, Xiangyan Wang, Zhipeng Qi, Yujie Yan, Jinghua Wang, Hongyuan Song, Hui Yang, Luguo Jin, Zhengyi Yang, Xiaoning Yang, Xiumei Kang, Xinfeng Liu, Zhuming Zhang, Chao Wang

{"title":"HDAC11 in ovarian granulosa cells coordinates LH in the maturation of oocytes in Tan sheep.","authors":"Jiaqi Shi, Donghuan Lv, Yaxiu Xu, Xiangyan Wang, Zhipeng Qi, Yujie Yan, Jinghua Wang, Hongyuan Song, Hui Yang, Luguo Jin, Zhengyi Yang, Xiaoning Yang, Xiumei Kang, Xinfeng Liu, Zhuming Zhang, Chao Wang","doi":"10.3724/abbs.2025036","DOIUrl":"https://doi.org/10.3724/abbs.2025036","url":null,"abstract":"Oocyte maturation plays an important role in supporting mammalian reproduction. Histone deacetylase 11 (HDAC11), the only member of the class IV histone deacetylase family and the smallest histone deacetylases (HDACs), has been shown to regulate oocyte maturation in mice and pigs. However, the epigenetic effects of HDACs in follicular granulosa cells in response to LH induction remain elusive in sheep. In this study, the effects of follicular somatic cell-derived HDAC11 on oocyte maturation in Tan sheep are evaluated. The expression changes of HDAC11 and related proteins are detected by means of immunofluorescence, immunohistochemistry, western blot analysis and enzyme-linked immunosorbent assay. Our results indicate that the level of HDAC11 in follicular granulosa cells as well as oocytes in Tan sheep increases with the growth and maturation of the follicles. Specific inhibition of HDAC11 by SIS17 remarkably reduces the oocyte maturation rate under LH supplementation in vitro. Accordingly, the acetylation level of H3K9 in granulosa cells is increased, while the EGF-like growth factor AREG is remarkably decreased. Furthermore, inhibition of HDAC11 markedly decreases the level of YAP1, which is a negative regulator of AREG in granulosa cells. Conclusively, HDAC11 in the granulosa cells of Tan sheep contributes to the LH induced production of AREG during oocyte in vitro maturation by decreasing the level of H3K9 acetylation and increasing the level of YAP1.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596088","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

AKR1C3 protects cardiomyocytes against hypoxia-induced cell apoptosis through the Nrf-2/NF-κB pathway. AKR1C3通过Nrf-2/NF-κB途径保护心肌细胞免受缺氧诱导的细胞凋亡。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-07 DOI: 10.3724/abbs.2024230

Wenlu Zhang, Wei Tian, Xin Xia, Hua Tian, Ting Sun

{"title":"AKR1C3 protects cardiomyocytes against hypoxia-induced cell apoptosis through the Nrf-2/NF-κB pathway.","authors":"Wenlu Zhang, Wei Tian, Xin Xia, Hua Tian, Ting Sun","doi":"10.3724/abbs.2024230","DOIUrl":"https://doi.org/10.3724/abbs.2024230","url":null,"abstract":"Hypoxia-induced apoptosis plays a critical role in the progression of various cardiac diseases, such as heart failure and acute myocardial infarction (AMI). Aldosterone reductase 1C3 (AKR1C3), a member of the aldo-keto reductase superfamily, participates in the metabolism of steroid hormones and redox reactions in vivo. Imbalances in prostaglandin levels have been linked to coronary events. However, the function and molecular mechanism by which AKR1C3 influences AMI are not yet fully understood. This study aims to investigate the role of AKR1C3 in hypoxia-induced myocardial cell damage and elucidate its mechanism. Our findings reveal that a hypoxic microenvironment triggers cardiomyocyte apoptosis and elevates AKR1C3 expression in H9C2 and AC16 cells, as well as in cardiac tissue from rats and mice with AMI. The overexpression of AKR1C3 promotes cardiomyocyte proliferation and cell vitality, whereas the silencing of AKR1C3 exerts the opposite effects in vitro. AKR1C3 protects cardiomyocytes against hypoxia-induced cell apoptosis by reducing ROS levels, preventing mitochondrial damage, and maintaining the oxygen consumption rate (OCR) and ATP production; conversely, AKR1C3 knockdown leads to adverse outcomes. Moreover, the application of a ROS inhibitor (MitoQ10) mitigates the increase in mitochondrial ROS in cardiomyocytes induced by AKR1C3 knockdown under hypoxic conditions. Mechanically, AKR1C3 increases Nrf-2 expression through the ubiquitin-proteasome pathway in cardiomyocytes and subsequently inhibits the NF-κB signaling pathway, thereby inhibiting Bax/caspase-3 signaling. Collectively, these results suggest that AKR1C3 prevents hypoxia-induced cardiomyocyte injury by modulating the Nrf-2/NF-κB axis, suggesting new insights into the mechanisms underlying myocardial protection.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584248","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

Exosomal integrin alpha 3 promotes epithelial ovarian cancer cell migration via the S100A7/p-ERK signaling pathway. 外泌体整合素- 3通过S100A7/p-ERK信号通路促进上皮性卵巢癌细胞迁移。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-07 DOI: 10.3724/abbs.2025024

Zeyuan Yin, Jiachen Ma, Joseph Adu-Amankwaah, Guangyan Xie, Yinghao Wang, Wei Tai, Zhenquan Sun, Chuting Huang, Guanfeng Chen, Tong Fu, Bei Zhang, Xueyan Zhou

{"title":"Exosomal integrin alpha 3 promotes epithelial ovarian cancer cell migration via the S100A7/p-ERK signaling pathway.","authors":"Zeyuan Yin, Jiachen Ma, Joseph Adu-Amankwaah, Guangyan Xie, Yinghao Wang, Wei Tai, Zhenquan Sun, Chuting Huang, Guanfeng Chen, Tong Fu, Bei Zhang, Xueyan Zhou","doi":"10.3724/abbs.2025024","DOIUrl":"https://doi.org/10.3724/abbs.2025024","url":null,"abstract":"Epithelial ovarian cancer (EOC) is a highly aggressive malignancy with a poor prognosis due to late-stage diagnosis and the lack of reliable biomarkers for early detection. Exosomes, small vesicles involved in intercellular communication, play a critical role in cancer progression by promoting migration, proliferation, and metastasis. This study investigates the role of exosomal proteins in EOC cell migration and identifies potential biomarkers. Exosomes are isolated from the ascites fluid of EOC patients (C-Exos) and benign ovarian disease patients (B-Exos), and mass spectrometry analysis of clinical samples reveals 185 differentially expressed proteins, with integrin alpha 3 (ITGA3) being strongly associated with poor prognosis. ITGA3 is transported via exosomes to recipient EOC cells, where it is released into the cytoplasm and translocated to the cell membrane. This localization enables ITGA3 to activate the intracellular signaling pathways that drive EOC migration. Immunoprecipitation mass spectrometry of clinical samples reveals that ITGA3 may influence EOC migration through the S100A7/p-ERK signaling pathway. Mechanistically, ITGA3 activates ERK signaling through S100A7, promoting cell migration. In vivo, exosomes enrich with ITGA3 facilitates tumor growth and migration, whereas ITGA3 knockdown reduces these effects. These findings suggest that exosomal ITGA3, via the S100A7/p-ERK signaling pathway, promotes EOC cell migration. ITGA3 could serve as a prognostic biomarker and therapeutic target in EOC. Targeting the ITGA3/S100A7 axis may help suppress migration, suggesting a promising strategy to improve EOC patient outcomes.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584254","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

Gastrodin inhibits reactive astrocyte-mediated inflammation in hypoxic-ischemic brain damage through S100B/RAGE-Smad3 signaling. 天麻素通过S100B/RAGE-Smad3信号抑制星形胶质细胞介导的缺氧缺血性脑损伤炎症反应。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-07 DOI: 10.3724/abbs.2024235

Pengxiang Wang, Hanjun Zuo, Haolong Shi, Zhao Wang, Xueqi Ren, Jinsha Shi, Tao Guo, Xianfeng Kuang, Min Zhao, Jinghui Li, Juanjuan Li

{"title":"Gastrodin inhibits reactive astrocyte-mediated inflammation in hypoxic-ischemic brain damage through S100B/RAGE-Smad3 signaling.","authors":"Pengxiang Wang, Hanjun Zuo, Haolong Shi, Zhao Wang, Xueqi Ren, Jinsha Shi, Tao Guo, Xianfeng Kuang, Min Zhao, Jinghui Li, Juanjuan Li","doi":"10.3724/abbs.2024235","DOIUrl":"https://doi.org/10.3724/abbs.2024235","url":null,"abstract":"Activated astrocytes and their associated inflammatory responses play critical roles in the pathogenesis of hypoxic-ischemic brain damage (HIBD). Gastrodin (GAS), an anti-inflammatory herbal agent, is known to suppress microglial activation. Here, we investigate whether it exerts a similar effect on activated astrocytes and whether it acts through S100B/RAGE-Smad3 signaling. The expression changes of S100B/RAGE-Smad3 signaling pathway-related proteins, inflammatory factors and A1/A2 astrocyte markers were detected by ELISA, western blot analysis, immunofluorescence and immunohistochemistry. The results show that GAS decreases the expression of sRAGE in the brain tissue and S100B in the serum and brain tissue of HIBD mice. However, it promotes the expression of sRAGE in the serum of HIBD mice. Moreover, GAS inhibits the expressions of RAGE, p-Smad3, TNF-α, and C3 (A1 astrocyte marker), and promotes the expressions of S100A10 (A2 astrocyte marker) and BDNF in HIBD model mice, as well as in oxygen glucose deprivation (OGD)-treated TNC-1 astrocytes. The immunofluorescence and immunohistochemical results of RAGE and p-Smad3, as well as the immunofluorescence results of C3 and S100A10, reveal the same trend. Interestingly, FPS-ZM1 (a specific inhibitor of RAGE) inhibits the expressions of p-Smad3, TNF-α, C3, and S100A10, but promotes that of BDNF compared with those in the OGD group. The combination of GAS and FPS-ZM1 further decreases the expression of C3. These results indicate that GAS can inhibit the activation of Smad3 through S100B/RAGE signaling and regulate the expression of A1/A2-type astrocytes.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584257","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

circ_0000389 inhibits intervertebral disc degeneration by targeting the miR-346/KLF7 axis. circ_0000389通过靶向miR-346/KLF7轴抑制椎间盘退变。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-07 DOI: 10.3724/abbs.2025029

Chun Liu, Cheng Yu, Yang Duan, Jianjun Li, Xiang Chen, Wenning Xu, Sujun Qiu

{"title":"circ_0000389 inhibits intervertebral disc degeneration by targeting the miR-346/KLF7 axis.","authors":"Chun Liu, Cheng Yu, Yang Duan, Jianjun Li, Xiang Chen, Wenning Xu, Sujun Qiu","doi":"10.3724/abbs.2025029","DOIUrl":"https://doi.org/10.3724/abbs.2025029","url":null,"abstract":"Intervertebral disc degeneration (IVDD) is a major cause of low back pain. An increasing number of studies have demonstrated that circRNAs regulate the progression of IVDD. However, the specific role of circ_0000389 in the progression of IVDD is not clear. In this study, circ_0000389 is selected by bioinformatics analysis of the GSE67566 dataset. RT-qPCR is performed to detect the expressions of circ_0000389, miR-346 and KLF7 in nucleus pulposus (NP) tissues. The proliferative capacity of nucleus pulposus cells (NPCs) is examined via CCK-8 assay. Western blot analysis of extracellular matrix (ECM) catabolism is performed in NPCs. Dual-luciferase reporter gene assays and RNA immunoprecipitation (RIP) confirm the interaction of circ_0000389 with miR-346 and KLF7. The expression of circ_0000389 is significantly downregulated in degenerating NP tissues. Functionally, circ_0000389 inhibits ECM catabolism. Mechanistically, we identify miR-346 and KLF7 as downstream target genes of circ_0000389 and miR-346, respectively. miR-346 overexpression reverses the effect of circ_0000389 on NPCs, and KLF7 overexpression reverses the effect of miR-346 on NPCs, indicating that circ_0000389 alleviates IVDD progression by regulating the miR-346/KLF7 axis. This study may provide a new therapeutic target for the treatment of IVDD.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584251","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

ISGylation: is our genome yearning for such a modification? isg酰化：我们的基因组渴望这样的修饰吗？

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-02-28 DOI: 10.3724/abbs.2025028

Zheng Chen, Zheng Li, Ying Wang, Zaure Dushimova, Kapanova Gulnara, Shunichi Takeda, Zhongjun Zhou, Xingzhi Xu

引用次数: 0

Iron overload mediates cytarabine resistance in AML by inhibiting the TP53 signaling pathway. 铁超载通过抑制TP53信号通路介导AML中的阿糖胞苷耐药。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-02-28 DOI: 10.3724/abbs.2025027

Yan Jia, Ling Li, Ying Li, Xunxun Zhu, Haiyan Wang, Bin Xu, Qiuping Li, Hao Zhang

{"title":"Iron overload mediates cytarabine resistance in AML by inhibiting the TP53 signaling pathway.","authors":"Yan Jia, Ling Li, Ying Li, Xunxun Zhu, Haiyan Wang, Bin Xu, Qiuping Li, Hao Zhang","doi":"10.3724/abbs.2025027","DOIUrl":"https://doi.org/10.3724/abbs.2025027","url":null,"abstract":"Currently, chemotherapy remains the primary treatment for acute myeloid leukemia (AML). Drug resistance in AML cells is a critical factor contributing to the failure of chemotherapy remission and subsequent relapse. Iron overload frequently occurs in AML patients because of hematopoietic suppression or supportive blood transfusion therapy. Previous studies have indicated that iron overload may promote the progression of AML; however, the underlying mechanisms remain unclear. Our results demonstrate that, compared with TP53-wild-type AML cells, TP53-mutant AML cells exhibit increased resistance to cytarabine-induced cytotoxicity. Moreover, reducing TP53 expression in wild-type AML cells diminishes their sensitivity to cytarabine. The TP53 signaling pathway is essential for mediating cytarabine-induced apoptosis in AML cells. In this study, an iron overload model in AML cells via the use of ferric citrate is constructed. Our data indicate that iron overload can suppress the TP53/BCL2/BAX signaling pathway, counteracting cytarabine-induced apoptosis. In TP53 wild-type AML cells, TFR1 participates in iron-mediated resistance to cytarabine by regulating the entry of iron into the cells. These findings provide a foundation for further exploration of the molecular mechanisms involved in AML resistance to cytarabine.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":"57 4","pages":"646-655"},"PeriodicalIF":3.3,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12040743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0