Acta biochimica et biophysica Sinica最新文献

CRATS: a one-pot CRISPR-Cas12b and RPA combined assay with a temperature switchcong for highly sensitive detection of monkeypox virus. CRATS：一种带有温度开关的单锅CRISPR-Cas12b和RPA联合试验，用于高灵敏度检测猴痘病毒。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-07 DOI: 10.3724/abbs.2025016

Guangxi Yu, Yue Wang, Yukang Chen, Jiangyuan Liu, Hongtao Kang, Xiaodong Luan, Song Gao, Pei Wang

引用次数: 0

miR-32-5p suppresses the progression of hepatocellular carcinoma by regulating the GSK3β/NF-κB signaling. miR-32-5p通过调控GSK3β/NF-κB信号通路抑制肝癌的进展。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-02 DOI: 10.3724/abbs.2025038

Guangzhi Wang, Qianqian Yang, Yaqi Han, Yunlong Zhang, Wei Pan, Zhongliang Ma, Hui Tian, Xudong Qu

{"title":"miR-32-5p suppresses the progression of hepatocellular carcinoma by regulating the GSK3β/NF-κB signaling.","authors":"Guangzhi Wang, Qianqian Yang, Yaqi Han, Yunlong Zhang, Wei Pan, Zhongliang Ma, Hui Tian, Xudong Qu","doi":"10.3724/abbs.2025038","DOIUrl":"https://doi.org/10.3724/abbs.2025038","url":null,"abstract":"Hepatocellular carcinoma (HCC) is a highly fatal form of malignancy that seriously threatens patient survival. The global 5-year survival rate for HCC patients ranges from 15% to 19%, and nearly 80% of patients are diagnosed at an advanced stage. Therefore, exploring the mechanism of HCC development and identifying biomarkers and therapeutic targets for HCC are vital. MicroRNAs (miRNAs), a class of noncoding single-stranded RNAs, are 20-24 nucleotides (nt) long. They play pivotal roles in modulating the progression of diverse diseases. The specific role of miR-32-5p in the development of HCC remains unclear. In this study, qRT-PCR is utilized to precisely determine the downregulated expression levels of miR-32-5p in HCC. Subsequently, functional analysis reveals the suppressive role of miR-32-5p in modulating the proliferative and migratory capabilities of HCC cells. Glycogen synthase kinase 3β (GSK3β) has emerged as a potential target of miR-32-5p, which is confirmed through a dual-luciferase reporter assay. Notably, the expression of GSK3β in HCC tissue specimens is negatively correlated with the abundance of miR-32-5p, and patients with high GSK3β expression have shorter survival time. Furthermore, the targeted downregulation of GSK3β remarkably impedes the proliferation and migration of tumor cells. This study suggests that miR-32-5p inhibits the proliferation and migration of HCC through regulating the GSK3β/NF-κB signaling pathway. Therefore, this study reveals that miR-32-5p exerts its suppressive effect on HCC progression, suggesting that it is a promising target for both diagnostic and targeted therapeutic interventions against HCC.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762648","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

TLR4 mediates lipotoxic β-cell dysfunction by inhibiting the TMEM24/PI3K/AKT pathway. TLR4通过抑制TMEM24/PI3K/AKT通路介导脂毒性β细胞功能障碍。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-02 DOI: 10.3724/abbs.2025045

Chao Lan, Yan Li, Zhiyan Weng, Wei Pan, Wanxin Lin, Zhen Jiang, Liyong Yang, Ximei Shen

{"title":"TLR4 mediates lipotoxic β-cell dysfunction by inhibiting the TMEM24/PI3K/AKT pathway.","authors":"Chao Lan, Yan Li, Zhiyan Weng, Wei Pan, Wanxin Lin, Zhen Jiang, Liyong Yang, Ximei Shen","doi":"10.3724/abbs.2025045","DOIUrl":"https://doi.org/10.3724/abbs.2025045","url":null,"abstract":"Immune imbalance is the core pathophysiological mechanism of the deterioration of β-cell function driven by lipid metabolism disorders. Toll-like receptor 4 (TLR4) inflammatory signaling is a key pathway that mediates lipotoxic injury in β-cells, but the underlying mechanism needs to be further elucidated. Transmembrane protein 24 (TMEM24) is a key transporter that regulates pulsatile insulin secretion, but its pathophysiology in lipotoxicity remains unclear. In this study, we investigate whether TLR4-mediated lipotoxicity is affected by the inhibition of TMEM24 expression. The PPI network shows that TLR4 is associated with both insulin secretion and ER stress proteins in islets from obese rats. Using in vitro lipotoxic β-cell models, we found that TMEM24 is the target signal of palmitic acid (PA)-induced insulin secretion impairment in islet β-cells, and TLR4 plays a mediating role in this process. Mechanistically, TLR4 mediates lipotoxicity by binding to TMEM24 and downregulating its protein expression to suppress PI3K/AKT signaling, leading to β-cell dysfunction. TLR4 knockout ameliorates islet function impairment through TMEM24/PI3K/AKT signaling in HFD-induced obese rats. Taken together, our results show that TLR4 mediates lipotoxicity in islet β-cells by inhibiting the TMEM24/PI3K/AKT pathway, and the mechanism of TLR4-mediated lipotoxicity is elucidated from the perspective of insulin vesicular secretion.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762697","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

In vitro and in vivo efficacy of aurintricarboxylic acid against Neospora caninum infection. 金羧酸抗犬新孢子虫感染的体内外疗效观察。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-31 DOI: 10.3724/abbs.2025006

Zhengkai Wei, Yuxiao Qian, Xi Jiang, Yuqian Jiang, Rongsheng Huang, Kaifeng He, Jing Huang, Jiaxuan Wang, Xin Guo, Wenlong Huang, Dezhi Zhang, Zhengtao Yang, Quan Liu, Qianyong Li

{"title":"In vitro and in vivo efficacy of aurintricarboxylic acid against Neospora caninum infection.","authors":"Zhengkai Wei, Yuxiao Qian, Xi Jiang, Yuqian Jiang, Rongsheng Huang, Kaifeng He, Jing Huang, Jiaxuan Wang, Xin Guo, Wenlong Huang, Dezhi Zhang, Zhengtao Yang, Quan Liu, Qianyong Li","doi":"10.3724/abbs.2025006","DOIUrl":"https://doi.org/10.3724/abbs.2025006","url":null,"abstract":"Bovine neosporosis, a protozoal disease caused by Neospora caninum ( N. caninum), poses a significant threat to the global cattle industry, resulting in substantial economic losses that are difficult to quantify. The current lack of effective commercial vaccines and specific treatments highlights the urgent need for the development of potent drugs against N. caninum. In this study, we investigate the efficacy of aurintricarboxylic acid (ATA), a derivative of polyaromatic carboxylic acid, against N. caninum both in vitro and in vivo. Cell cytotoxicity is evaluated using CCK-8 kits. N. caninum proliferation within cells is assessed by qPCR analysis. Transmission electron microscopy (TEM) is employed to examine the ultrastructures of N. caninum tachyzoites. The efficacy of ATA against N. caninum infection is validated in a mouse model. Our findings indicate that ATA not only inhibits N. caninum proliferation but also reduces parasite loads within individual cells. Furthermore, ATA (20 and 40 μM) has immunomodulatory effects by downregulating the mRNA expressions of N . caninum-induced cytokines, including tumor necrosis factor-α (TNF-α), interferon (IFN-α, -β, and -γ), and β-defensin 5 (BNBD5). ATA treatment directly targets and eliminates N. caninum by disrupting its ultrastructure. The in vivo study confirms the potential of ATA to increase body weight, decrease parasite loads in the lungs and duodenum, and ameliorate the pathological effects induced by N . caninum infection in mice. In conclusion, this study represents the first evidence of the anti- N. caninum ability of ATA and provides compelling data to support its potential as a candidate for developing anti- N. caninum drugs.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143750539","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

TRIM21 promotes type I interferon by inhibiting the autophagic degradation of STING via p62/SQSTM1 ubiquitination in systemic lupus erythematosus. TRIM21在系统性红斑狼疮中通过p62/SQSTM1泛素化抑制STING的自噬降解，从而促进I型干扰素的产生。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-31 DOI: 10.3724/abbs.2025046

Chen Li, Ang Ma, Yu Bai, Zitao Liu, Linghan Tian, Ziyuan Wang, Huaishun Ma, Zhengpu Chen, Zhengheng Gao, Shijie Feng, Ping Fu

{"title":"TRIM21 promotes type I interferon by inhibiting the autophagic degradation of STING via p62/SQSTM1 ubiquitination in systemic lupus erythematosus.","authors":"Chen Li, Ang Ma, Yu Bai, Zitao Liu, Linghan Tian, Ziyuan Wang, Huaishun Ma, Zhengpu Chen, Zhengheng Gao, Shijie Feng, Ping Fu","doi":"10.3724/abbs.2025046","DOIUrl":"https://doi.org/10.3724/abbs.2025046","url":null,"abstract":"The cGAS-STING signaling pathway serves as a pivotal surveillance mechanism for cytosolic double-stranded DNA (dsDNA) detection in mammalian systems. While STING-mediated type I interferon production is crucial for host defense, sustained activation of this pathway contributes to autoimmune pathologies, including systemic lupus erythematosus (SLE). Maintaining immune homeostasis requires precise regulation of STING activity to prevent hyperactivation. Our study identifies TRIM21 as a novel positive regulator of cGAS-STING signaling in SLE pathogenesis. Our results demonstrate that TRIM21 overexpression stabilizes STING by suppressing autophagic degradation, whereas TRIM21 depletion accelerates this clearance process. Mechanistically, TRIM21 catalyzes the K63-linked polyubiquitylation of the selective autophagy receptor p62/SQSTM1, disrupting its interaction with STING. This post-translational modification prevents the sequestration of STING into autophagosomes, thereby stabilizing the adaptor protein and amplifying downstream type I interferon responses. Our findings reveal a previously unrecognized regulatory circuit in which TRIM21 orchestrates cross-talk between ubiquitin signaling and autophagy to control STING turnover. The TRIM21-p62 axis represents a potential therapeutic target for attenuating pathological interferon production in STING-dependent autoimmune disorders. This work advances our understanding of immune regulation by demonstrating how E3 ligase-mediated ubiquitin modifications modulate cargo recognition in selective autophagy pathways. The identified mechanism provides new insights into the molecular interplay between protein ubiquitylation and autophagic degradation in maintaining the innate immune balance, offering novel perspectives for developing targeted therapies against interferonopathies associated with cGAS-STING hyperactivity.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143750541","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

Breast cancer-derived exosomal miR-105-5p facilitates the transformation of NFs into CAFs through LATS2-NF-κB signaling. 乳腺癌来源的外泌体miR-105-5p通过LATS2-NF-κB信号传导促进NFs向CAFs的转化。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-28 DOI: 10.3724/abbs.2025017

Xiaodi Ding, Zhimei Sheng, Jiayu Cui, Meimei Cui, Liying Zhang, Ruijun Feng, Yongming Wang, Wei Sun, Xiurong Zhang, Lihong Shi, Baogang Zhang

{"title":"Breast cancer-derived exosomal miR-105-5p facilitates the transformation of NFs into CAFs through LATS2-NF-κB signaling.","authors":"Xiaodi Ding, Zhimei Sheng, Jiayu Cui, Meimei Cui, Liying Zhang, Ruijun Feng, Yongming Wang, Wei Sun, Xiurong Zhang, Lihong Shi, Baogang Zhang","doi":"10.3724/abbs.2025017","DOIUrl":"https://doi.org/10.3724/abbs.2025017","url":null,"abstract":"Studies of cell-to-cell activities in the tumor microenvironment (TME) have identified multiple potential targets for oncotherapy. The interplay between tumor cells and neighboring cancer-associated fibroblasts (CAFs) persists in all stages of tumor progression. In this study, we reveal that exosomes from breast cancer cells can be endocytosed into fibroblasts and transform normal fibroblasts (NFs) into CAFs and that the ability of exosomes from highly metastatic breast cancer cells is greater than that of those from poorly metastatic breast cancer cells. Further investigation reveals that exosomes from highly metastatic breast cancer cells contain much more miR-105-5p than those from poorly metastatic breast cells do and that exosomal miR-105-5p facilitates the transformation of NFs to CAFs. A detailed study reveals that RBMY1A1-dependent sorting of miR-105-5p into fibroblasts and subsequent internalization of miR-105-5p promote the transformation of NFs to CAFs by downregulating LATS2 expression and activating NF-κB signaling, which concurrently facilitates the EMT of breast cancer cells. Thus, our results indicate that exosomal miR-105-5p may be a potential target for novel therapeutic strategies to prevent the coevolution of breast cancer cells and CAFs.","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":"143727338","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

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