Acta biochimica et biophysica Sinica最新文献_第3页

Corrigendum to: TIPE1 suppresses the invasion and migration of breast cancer cells and inhibits epithelial-to-mesenchymal transition primarily via the ERK signaling pathway. 更正：TIPE1TIPE1 主要通过 ERK 信号通路抑制乳腺癌细胞的侵袭和迁移，并抑制上皮细胞向间质转化。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-10-09 DOI: 10.3724/abbs.2024177

Shusheng Qiu, Wei Hu, Qiuhong Ma, Yi Zhao, Liang Li, Yu Ding

引用次数: 0

The biogenesis, regulation and functions of transitive siRNA in plants. 植物中转基因 siRNA 的生物发生、调控和功能。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-10-08 DOI: 10.3724/abbs.2024160

Huijun Tan, Yuelin Liu, Hongwei Guo

{"title":"The biogenesis, regulation and functions of transitive siRNA in plants.","authors":"Huijun Tan, Yuelin Liu, Hongwei Guo","doi":"10.3724/abbs.2024160","DOIUrl":"https://doi.org/10.3724/abbs.2024160","url":null,"abstract":"Small RNA (sRNA)-mediated RNA interference (RNAi) is a sequence-specific gene silencing mechanism that modulates gene expression in eukaryotes. As core molecules of RNAi, various sRNAs are encoded in the plant genome or derived from invading RNA molecules, and their biogenesis depends on distinct genetic pathways. Transitive small interfering RNAs (siRNAs), which are sRNAs produced from double-strand RNA (dsRNA) in a process that depends on RNA-dependent RNA polymerases (RDRs), can amplify and spread silencing signals to additional transcripts, thereby enabling a phenomenon termed \"transitive RNAi\". Members of this class of siRNAs function in various biological processes ranging from development to stress adaptation. In Arabidopsis thaliana, two RDRs participate in the generation of transitive siRNAs, acting cooperatively with various siRNA generation-related factors, such as the RNA-induced silencing complex (RISC) and aberrant RNAs. Transitive siRNAs are produced in diverse subcellular locations and structures under the control of various mechanisms, highlighting the intricacies of their biogenesis and functions. In this review, we discuss recent advances in understanding the molecular events of transitive siRNA biogenesis and its regulation, with a particular focus on factors involved in RDR recruitment. We aim to provide a comprehensive description of the generalized mechanism governing the biogenesis of transitive siRNAs. Additionally, we present an overview of the diverse biological functions of these siRNAs and raise some pressing questions in this area for further investigation.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142387214","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

HADHA promotes esophageal cancer progression by activating mTOR signaling and the SP1/MDM2 axis. HADHA 通过激活 mTOR 信号和 SP1/MDM2 轴促进食管癌的进展。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-09-27 DOI: 10.3724/abbs.2024139

Xusheng Ding, Longlong Shao, Jie Wang, Yongwei Jin, Haiqing Chen, Bin Li

{"title":"HADHA promotes esophageal cancer progression by activating mTOR signaling and the SP1/MDM2 axis.","authors":"Xusheng Ding, Longlong Shao, Jie Wang, Yongwei Jin, Haiqing Chen, Bin Li","doi":"10.3724/abbs.2024139","DOIUrl":"https://doi.org/10.3724/abbs.2024139","url":null,"abstract":"Esophageal cancer (EC) is one of the most recalcitrant cancers, with a 5-year survival rate of <30%. The hydroxyacyl-CoA dehydrogenase alpha subunit (HADHA) plays an essential role in long-chain fatty acid metabolism, and dysregulation of HADHA has been demonstrated to be involved in a series of metabolic diseases and cancers. However, its role in cancers remains controversial. HADHA has seldom been investigated in EC, and little is known about how HADHA regulates the malignant progression of EC. In this study, we find that HADHA is significantly upregulated in EC tissues and is correlated with poor survival. HADHA knockdown markedly inhibits EC cell proliferation both in vitro and in vivo. The loss of HADHA also induces EC cell apoptosis, causes cell cycle arrest and inhibits cell migration. Additionally, RNA profiling reveals that mTOR signaling is significantly suppressed after HADHA knockdown. Mechanistically, HADHA interacts with SP1 and induces MDM2 expression. In conclusion, both mTOR signaling and the SP1-MDM2 axis participate in the HADHA-induced malignant behavior of EC cells.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339041","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

RNA methylation in neurodevelopment and related diseases. 神经发育和相关疾病中的 RNA 甲基化。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-09-27 DOI: 10.3724/abbs.2024159

Wenjuan Xia, Yue Liu, Jiafeng Lu, Hoi-Hung Cheung, Qingxia Meng, Boxian Huang

引用次数: 0

Characterization of the association and sequestration of RNA-binding proteins by single-stranded DNA chimera. 单链 DNA 嵌合体对 RNA 结合蛋白的关联和封存的表征。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-09-26 DOI: 10.3724/abbs.2024157

Jianyang Wang, Wenliang Guan, Leilei Jiang, Hongyu Hu

引用次数: 0

UHRF1 knockdown induces cell cycle arrest and apoptosis in breast cancer cells through the ZBTB16/ANXA7/Cyclin B1 axis. UHRF1 基因敲除可通过 ZBTB16/ANXA7/Cyclin B1 轴诱导乳腺癌细胞的细胞周期停滞和细胞凋亡。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-09-23 DOI: 10.3724/abbs.2024148

Di Liu, Qin Du, Yuxuan Zhu, Yize Guo, Ya Guo

{"title":"UHRF1 knockdown induces cell cycle arrest and apoptosis in breast cancer cells through the ZBTB16/ANXA7/Cyclin B1 axis.","authors":"Di Liu, Qin Du, Yuxuan Zhu, Yize Guo, Ya Guo","doi":"10.3724/abbs.2024148","DOIUrl":"https://doi.org/10.3724/abbs.2024148","url":null,"abstract":"Ubiquitin-like containing PHD and RING finger domains 1 (UHRF1) is involved in tumorigenicity through DNA methylation in various cancers, including breast cancer. This study aims to investigate the regulatory mechanisms of UHRF1 in breast cancer progression. Herein, we show that UHRF1 is upregulated in breast cancer tissues and cell lines as measured by western blot analysis and immunohistochemistry. Breast cancer cells are transfected with a UHRF1 overexpression plasmid (pcDNA-UHRF1) or short hairpin RNA targeting UHRF1 (sh-UHRF1), followed by detection of cell proliferation, invasion, apoptosis, and cell cycle. UHRF1 overexpression promotes proliferation and invasion and attenuates cell cycle arrest and apoptosis in breast cancer cells, while UHRF1 knockdown shows the opposite effect. Moreover, methylation-specific PCR and ChIP assays indicate that UHRF1 inhibits zinc finger and BTB domain containing 16 (ZBTB16) expression by promoting ZBTB16 promoter methylation via the recruitment of DNA methyltransferase 1 (DNMT1). Then, a co-IP assay is used to verify the interaction between ZBTB16 and the annexin A7 (ANXA7) protein. ZBTB16 promotes ANXA7 expression and subsequently inhibits Cyclin B1 expression. Rescue experiments reveal that ZBTB16 knockdown reverses the inhibitory effects of UHRF1 knockdown on breast cancer cell malignancies and that ANXA7 knockdown abolishes the inhibitory effects of ZBTB16 overexpression on breast cancer cell malignancies. Additionally, UHRF1 knockdown significantly inhibits xenograft tumor growth in vivo. In conclusion, UHRF1 knockdown inhibits proliferation and invasion, induces cell cycle arrest and apoptosis in breast cancer cells via the ZBTB16/ANXA7/Cyclin B1 axis, and reduces xenograft tumor growth in vivo.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142278636","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

Unveiling the cytotoxicity of a new gold(I) complex towards hepatocellular carcinoma by inhibiting TrxR activity. 通过抑制 TrxR 活性揭示新型金（I）复合物对肝细胞癌的细胞毒性。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-09-20 DOI: 10.3724/abbs.2024155

Yuan Wang, Haokun Yuan, Ruiqin Fang, Ran Zhang, Wei-Jia Wang

{"title":"Unveiling the cytotoxicity of a new gold(I) complex towards hepatocellular carcinoma by inhibiting TrxR activity.","authors":"Yuan Wang, Haokun Yuan, Ruiqin Fang, Ran Zhang, Wei-Jia Wang","doi":"10.3724/abbs.2024155","DOIUrl":"10.3724/abbs.2024155","url":null,"abstract":"Hepatocellular carcinoma (HCC), the predominant type of liver cancer, is an aggressive malignancy with limited therapeutic options. In this study, we assess a collection of newly designed gold(I) phosphine complexes. Remarkably, the compound GC002 exhibits the greatest toxicity to HCC cells and outperforms established medications, such as sorafenib and auranofin, in terms of antitumor efficacy. GC002 triggers irreversible necroptosis in HCC cells by increasing the intracellular accumulation of reactive oxygen species (ROS). Mechanistically, GC002 significantly suppresses the activity of thioredoxin reductase (TrxR), which plays a crucial role in regulating redox homeostasis and is often overexpressed in HCC by binding directly to the enzyme. Our in vivo xenograft study confirms that GC002 possesses remarkable antitumor activity against HCC without severe side effects. These findings not only highlight the novel mechanism of controlling necroptosis via TrxR and ROS but also identify GC002 as a promising candidate for the further development of antitumor agents targeting HCC.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11532207/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142306914","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

Label-free and rapid mechanics of single cells under high-density co-culture conditions by deep learning image recognition-assisted atomic force microscopy. 通过深度学习图像识别辅助原子力显微镜，对高密度共培养条件下的单细胞进行无标记快速力学研究。

IF 3.7 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-09-19 DOI: 10.3724/abbs.2024158

Xuliang Yang,Mi Li

引用次数: 0

miR-155 induces sepsis-associated damage to the intestinal mucosal barrier via sirtuin 1/nuclear factor-κB-mediated intestinal pyroptosis. miR-155通过sirtuin 1/核因子-κB介导的肠道脓毒症诱导脓毒症相关的肠粘膜屏障损伤。

IF 3.7 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-09-12 DOI: 10.3724/abbs.2024124

Zhihua Li,Yi Wang,Weiwei Huang,Xingyu Shi,Tao Ma,Xiangyou Yu

{"title":"miR-155 induces sepsis-associated damage to the intestinal mucosal barrier via sirtuin 1/nuclear factor-κB-mediated intestinal pyroptosis.","authors":"Zhihua Li,Yi Wang,Weiwei Huang,Xingyu Shi,Tao Ma,Xiangyou Yu","doi":"10.3724/abbs.2024124","DOIUrl":"https://doi.org/10.3724/abbs.2024124","url":null,"abstract":"Sepsis is a life-threatening state of organ dysfunction caused by systemic inflammation and a dysfunctional response to host infections that can induce severe intestinal mucosal damage. Pyroptosis is mediated by the activated NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome after stimulation by various inflammatory factors during sepsis. The inflammatory response is a major driver of intestinal damage during sepsis. Intestinal mucosal barrier dysfunction in sepsis is associated with pyroptosis, a type of programmed inflammatory cell death. Several studies have confirmed the role of miR-155 in sepsis and other diseases. However, the effect of miR-155 on intestinal pyroptosis in the context of intestinal mucosal barrier dysfunction during sepsis remains unclear. Thus, a model of sepsis in Sprague-Dawley rats is established using cecal ligation and puncture (CLP), and a series of molecular biological methods are used in this study. The results show that the expression of miR-155 is increased and that of sirtuin 1 (SIRT1) is decreased in the intestinal tissues of patients with sepsis. miR-155 expression is negatively correlated with SIRT1 expression. Increased miR-155 expression significantly inhibits SIRT1 activity and upregulates the expressions of NOD-like receptor family pyrin domain-containing 3 (NLRP3), caspase-1, apoptosis-associated speck-like protein containing a CARD (ASC), interleukin-1β (IL-1β) and interleukin-18 (IL-18) to promote pyroptosis. The inhibition of miR-155 expression is associated with increased SIRT1 expression, promotes the deacetylation of p65, and significantly downregulates p65 acetylation. Herein, we propose that miR-155 induces pyroptosis in the intestine partly by regulating SIRT1, thereby reducing the deacetylation of the nuclear factor (NF)-κB subunit p65 and increasing NF-κB signaling activity in sepsis, leading to intestinal barrier damage.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142202358","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

Silencing of PCK1 mitigates the proliferation and migration of vascular smooth muscle cells and vascular intimal hyperplasia by suppressing STAT3/DRP1-mediated mitochondrial fission. 通过抑制 STAT3/DRP1 介导的线粒体裂变，沉默 PCK1 可减轻血管平滑肌细胞的增殖和迁移以及血管内膜增生。

IF 3.7 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-09-12 DOI: 10.3724/abbs.2024154

Li Zhang,Yingmei Chen,Quanrong Pan,Shizheng Fang,Zhongjian Zhang,Jia Wang,Yongjian Yang,Dachun Yang,Xiongshan Sun

{"title":"Silencing of PCK1 mitigates the proliferation and migration of vascular smooth muscle cells and vascular intimal hyperplasia by suppressing STAT3/DRP1-mediated mitochondrial fission.","authors":"Li Zhang,Yingmei Chen,Quanrong Pan,Shizheng Fang,Zhongjian Zhang,Jia Wang,Yongjian Yang,Dachun Yang,Xiongshan Sun","doi":"10.3724/abbs.2024154","DOIUrl":"https://doi.org/10.3724/abbs.2024154","url":null,"abstract":"The pathological proliferation and migration of vascular smooth muscle cells (VSMCs) are key processes during vascular neointimal hyperplasia (NIH) and restenosis. Phosphoenolpyruvate carboxy kinase 1 (PCK1) is closely related to a variety of malignant proliferative diseases. However, the role of PCK1 in VSMCs has rarely been investigated. This study aims to examine the role of PCK1 in the proliferation and migration of VSMCs and vascular NIH after injury. In vivo, extensive NIH and increased expression of PCK1 within the neointima are observed in injured arteries. Interestingly, the administration of adeno-associated virus-9 (AAV-9) carrying Pck1 short hairpin RNA (sh Pck1) significantly attenuates NIH and stenosis of the vascular lumen. In vitro, Pck1 small interfering RNA (si Pck1)-induced PCK1 silencing inhibits VSMC proliferation and migration. Additionally, silencing of PCK1 leads to reduced expression of dynamin-related protein 1 (DRP1) and attenuated mitochondrial fission. Lentivirus-mediated DRP1 overexpression markedly reverses the inhibitory effects of PCK1 silencing on VSMC proliferation, migration, and mitochondrial fission. Finally, PCK1 inhibition attenuates the phosphorylation of signal transducer and activator of transcription 3 (STAT3). Activation of STAT3 abolishes the suppressive effects of PCK1 silencing on DRP1 expression, mitochondrial fission, proliferation, and migration in VSMCs. In conclusion, PCK1 inhibition attenuates the mitochondrial fission, proliferation, and migration of VSMCs by inhibiting the STAT3/DRP1 axis, thereby suppressing vascular NIH and restenosis.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142202359","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