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

The role of cryptochrome (CRY) in cancer: molecular mechanisms and Clock-based therapeutic strategies.

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-19 DOI: 10.3724/abbs.2025025

Shuzhao Zhang, Xue Chen, Jiayi Li, Anan Xu, Ann M Bode, Xiangjian Luo

引用次数: 0

Antitumor potential of polyamines in cancer.

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-19 DOI: 10.3724/abbs.2025030

He Liu, Yi Liu, Xinyue Wang, Zhiwen Xiao, Quanxing Ni, Xianjun Yu, Guopei Luo

引用次数: 0

Histone acetylases are required for iron homeostasis in yeast.

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-17 DOI: 10.3724/abbs.2025040

Jian Zhang, Yong Xue, Xinya Zhang, Renjie Qi, Yaqi Zhang, Chen Lu, Zhidan Luo

引用次数: 0

Knockdown of lncRNA XR_877193.1 suppresses ferroptosis and promotes osteogenic differentiation via the PI3K/AKT signaling pathway in SONFH.

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-17 DOI: 10.3724/abbs.2025014

Huixia Yang, Ning Ding, Shi Qing, Yinju Hao, Cilin Zhao, Kai Wu, Guizhong Li, Huiping Zhang, Shengchao Ma, Zhigang Bai, Yideng Jiang

{"title":"Knockdown of lncRNA XR_877193.1 suppresses ferroptosis and promotes osteogenic differentiation via the PI3K/AKT signaling pathway in SONFH.","authors":"Huixia Yang, Ning Ding, Shi Qing, Yinju Hao, Cilin Zhao, Kai Wu, Guizhong Li, Huiping Zhang, Shengchao Ma, Zhigang Bai, Yideng Jiang","doi":"10.3724/abbs.2025014","DOIUrl":"https://doi.org/10.3724/abbs.2025014","url":null,"abstract":"Ferroptosis is a novel form of regulated cell death characterized by the iron-dependent accumulation of lipid peroxides. Recent research has suggested that ferroptosis in osteoblasts contributes to steroid-induced osteonecrosis of the femoral head (SONFH). However, the relationship between ferroptosis and SONFH remains unclear. In this study, in vitro experiments show that dexamethasone (Dex) treatment reduces the expressions of key ferroptosis regulators, SLC7A11 and GPX4, in MC3T3-E1 cells. This reduction leads to a decrease in intracellular glutathione (GSH) levels, accompanied by elevated levels of total iron, malondialdehyde (MDA), and reactive oxygen species (ROS). Importantly, the ferroptosis inhibitor ferrostatin-1 (Fer-1) effectively reverses Dex-induced ferroptosis in MC3T3-E1 cells. Furthermore, RNA-seq analysis reveals that the long noncoding RNA (lncRNA) XR_877193.1is significantly upregulated in Dex-treated MC3T3-E1 cells. Functional studies demonstrate that the knockdown of lncRNA XR_877193.1 promotes osteogenic differentiation by inhibiting Dex-induced ferroptosis in MC3T3-E1 cells, whereas its overexpression exacerbates cell death via ferroptosis. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis reveals that the differentially expressed lncRNA XR_877193.1 is enriched in ferroptosis-related pathways, including the PI3K/AKT signaling pathway. Moreover, PI3K/AKT inhibitors reverse ferroptosis in MC3T3-E1 cells inhibited by lncRNA XR_877193.1 knockdown. Collectively, our findings indicate that lncRNA XR_877193.1 knockdown exerts anti-ferroptosis effects by stimulating the PI3K/AKT signaling pathway, suggesting a promising therapeutic strategy for attenuating SONFH.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143646715","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 protective effect of naringenin on ulcerative colitis in mice through increasing Nrf2 pathway activity.

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-12 DOI: 10.3724/abbs.2025026

Jiaxiang Li, Li Hua, Meichun Hu, Ni Zhu, Sijin Dong, Xiaoli Jing, Zihuan Zhu, Yifei Liu, Yanhong Zhou

{"title":"The protective effect of naringenin on ulcerative colitis in mice through increasing Nrf2 pathway activity.","authors":"Jiaxiang Li, Li Hua, Meichun Hu, Ni Zhu, Sijin Dong, Xiaoli Jing, Zihuan Zhu, Yifei Liu, Yanhong Zhou","doi":"10.3724/abbs.2025026","DOIUrl":"https://doi.org/10.3724/abbs.2025026","url":null,"abstract":"Ulcerative colitis (UC) is a chronic inflammatory disease with an increasing prevalence worldwide. Naringenin (NAR) has been proven effective in preventing UC, but its mechanism has not been fully elucidated. In this study, network pharmacology and bioinformatics methods are used to screen the genes associated with NAR and UC. A mouse model of dextran sulfate sodium (DSS)-induced UC is established. After treatment with NAR, the disease activity index (DAI) is scored, and colonic histopathology is observed via hematoxylin-eosin (HE) staining. The expressions of the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway and inflammation-related factors in the colons of UC mice are examined via western blot analysis and immunohistochemistry (IHC). The results of the animal experiments reveal that the model group of UC mice present the most severe weight loss and the highest DAI scores. After the administration of NAR, weight loss is alleviated, and DAI scores are reduced ( P < 0.05). NAR improves pathological manifestations in the mouse colon, such as reducing inflammatory cell infiltration and restoring goblet cell loss ( P < 0.05). NAR significantly increases the protein expression levels of Nrf2, heme oxygenase 1 (HO-1), and NAD(P)H dehydrogenase [quinone] 1 (NQO1) in the colon ( P < 0.05) but decreases the protein expression levels of nuclear factor kappa-B (NF-κB), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) ( P < 0.05), thus alleviating the inflammatory response in UC model mice.","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":"143612905","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

PGC7 maintains the pluripotency of F9 embryonic carcinoma cells by promoting Nanog translation.

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.

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.

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.

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.

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