Acta biochimica et biophysica Sinica最新文献_第5页

A positive feedback loop between FOSB and miR-133b controls colon cancer cell proliferation. FOSB和miR-133b之间的正反馈回路控制着结肠癌细胞的增殖。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-28 DOI: 10.3724/abbs.2025041

Wanwan Li, Qionggui Hu, Changwei Lin, Xiaorong Li, Yang Bai, Min Ma

{"title":"A positive feedback loop between FOSB and miR-133b controls colon cancer cell proliferation.","authors":"Wanwan Li, Qionggui Hu, Changwei Lin, Xiaorong Li, Yang Bai, Min Ma","doi":"10.3724/abbs.2025041","DOIUrl":"https://doi.org/10.3724/abbs.2025041","url":null,"abstract":"FOSB, a member of the FOS gene family, forms heterodimers with JUN family proteins to engage in diverse cellular processes. Its biological impacts vary among different types of tumors, yet its specific function in colon cancer (CC) remains ambiguous. In this study, quantitative real-time PCR (qRT-PCR) and immunohistochemistry (IHC) are applied to measure FOSB expression levels, followed by an analysis of the association between FOSB expression and patients' clinical parameters. In vitro experiments are performed to assess cell proliferation, including growth rate, cell cycle distribution, and apoptosis. A subcutaneous xenograft model in nude mice is utilized to monitor tumor growth in vivo. Additionally, chromatin immunoprecipitation (ChIP) and luciferase reporter assays are conducted to dissect the interactions among FOSB, miR-133b, and POU2F1. The results indicate that FOSB expression is downregulated in CC tissues relative to normal controls. Overexpression of FOSB suppresses proliferation and promotes apoptosis in CC cells. Mechanistically, FOSB binds to the promoter region of miR-133b, enhancing its transcription and subsequently repressing POU2F1 expression. Notably, decreased POU2F1 expression also alleviates the transcriptional repression of the FOSB promoter region, establishing a FOSB-miR-133b-POU2F1 feedback loop that inhibits CC proliferation. In summary, our findings suggest that FOSB acts as a tumor suppressor gene in CC and may exert its inhibitory effects on CC growth via the FOSB-miR-133b-POU2F1 feedback loop.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143727337","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: Overexpression of PTEN induces cell growth arrest and apoptosis in human breast cancer ZR-75-1 cells. 更正：PTEN过表达诱导人乳腺癌ZR-75-1细胞生长阻滞和凋亡。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-25 DOI: 10.3724/abbs.2024244

Xiangyong Li, Guanping Lin, Binhua Wu, Xin Zhou, Keyuan Zhou

引用次数: 0

Corrigendum to: Excessive ER-phagy mediated by FAM134B contributes to trophoblast cell mitochondrial dysfunction in preeclampsia. 更正：FAM134B介导的过度er吞噬有助于子痫前期滋养细胞线粒体功能障碍。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-25 DOI: 10.3724/abbs.2025001

Andi Wang, Zhuo Li, Dan Zhang, Chang Chen, Hua Zhang

引用次数: 0

METTL3-mediated m ⁶A modification of pri-miRNA-31 promotes hypertrophic scar progression. mettl3介导的m6a修饰的pri-miRNA-31促进增生性疤痕进展。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-19 DOI: 10.3724/abbs.2025033

Qirui Wang, Jialin Hou, Siyi Zeng, Xue Wang, Yimin Liang, Renpeng Zhou

{"title":"METTL3-mediated m 6A modification of pri-miRNA-31 promotes hypertrophic scar progression.","authors":"Qirui Wang, Jialin Hou, Siyi Zeng, Xue Wang, Yimin Liang, Renpeng Zhou","doi":"10.3724/abbs.2025033","DOIUrl":"https://doi.org/10.3724/abbs.2025033","url":null,"abstract":"Hypertrophic scar (HS) is a pathological scar characterized by excessive dermal fibrosis. Aberrant m 6A modification patterns have been identified in HS; however, the expression of the methyltransferase, along with its function and molecular mechanisms in HS, remains unclear. In this study, we find that both the protein level of METTL3 and the level of m6A methylation are upregulated in HS compared with normal skin. To investigate the role of METTL3 in HS, we knock down METTL3 in HS-derived fibroblasts (HSFBs) via shRNA. METTL3 knockdown reduces the expressions of collagen types I and III (COL I/III) and α-SMA, inhibits cell proliferation and migration, and induces cell cycle arrest in the G1 phase. MeRIP-seq analysis reveals m 6A modification sites on pri-miR-31. Our data indicate that the expression level of pri-miR-31 is elevated in METTL3-knockdown HSFBs, whereas the level of mature miR-31-5p is reduced. Notably, transfection of a miR-31-5p mimic into HSFBs partially counteracts the inhibitory effects of the m 6A methylation inhibitors cycloleucine and STM2457 (a specific inhibitor of METTL3) on fibrosis and cellular proliferation. Additionally, we confirm that ZBTB20 is a downstream target of miR-31-5p and that knockdown of ZBTB20 inhibits fibroblast fibrosis. Collectively, our findings elucidate the epigenetic mechanism of METTL3/m 6A/pri-miR-31/ZBTB20 in HS fibrosis, providing a potential therapeutic target for HS.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143661939","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

Atrial APD prolongation caused by the upregulation of RAGE and subsequent I _NaL increase in diabetic patients. 糖尿病患者RAGE上调及随后I NaL升高引起心房APD延长

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-19 DOI: 10.3724/abbs.2025018

Yingchun Luo, Wenbo Ma, Qi Kang, Han Pan, Ling Shi, Jiudong Ma, Jiahui Song, Dongmei Gong, Kai Kang, Xuexin Jin

{"title":"Atrial APD prolongation caused by the upregulation of RAGE and subsequent I NaL increase in diabetic patients.","authors":"Yingchun Luo, Wenbo Ma, Qi Kang, Han Pan, Ling Shi, Jiudong Ma, Jiahui Song, Dongmei Gong, Kai Kang, Xuexin Jin","doi":"10.3724/abbs.2025018","DOIUrl":"https://doi.org/10.3724/abbs.2025018","url":null,"abstract":"Diabetes mellitus (DM) is a risk factor for the development of atrial fibrillation (AF). The action potential duration (APD) has been demonstrated to be prolonged in the atrium of diabetic mice. In contrast, the APD is generally shortened in AF patients. It is unclear what change occurs in the atrial APD of diabetic patients. In this study, we explore the APD change of atrial myocytes from diabetic patients and the underlying molecular mechanisms. The whole-cell patch-clamp technique is used to detect single-cell electrical activity in diabetic and nondiabetic human samples. The results show that both APD 50 and APD 90, the APD at 50% and 90% repolarization, are increased in diabetic patients compared with those in nondiabetic controls. The density of late sodium current ( I NaL) in the atrial myocytes of diabetic patients is greater than that in the myocytes of nondiabetic patients. The expression of receptor for advanced glycation end products (RAGE) is increased in the atria of diabetic patients. In cultured HL-1 cells, high glucose (HG) treatment increases I NaL, and the expression of RAGE prolongs APD. The siRNA-mediated knockdown of RAGE reduces the I NaL and shortens the APD. The APD is prolonged in the atria of diabetic patients because of the upregulation of RAGE and the subsequent increase in I NaL. Our findings provide novel insights into atrial electrical remodeling in diabetic patients.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143661932","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 role of cryptochrome (CRY) in cancer: molecular mechanisms and Clock-based therapeutic strategies. 隐色素（CRY）在癌症中的作用：分子机制和基于时钟的治疗策略。

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. 多胺在肿瘤中的抗肿瘤潜力。

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. 组蛋白乙酰化酶是酵母维持铁稳态所必需的。

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. lncRNA XR_877193.1的下调通过PI3K/AKT信号通路抑制SONFH中的铁下垂并促进成骨分化。

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. 柚皮素通过提高Nrf2通路活性对小鼠溃疡性结肠炎的保护作用。

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