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

Cx58 is associated with the metastasis of non-small cell lung cancer via MEF2B/Cx58 axis. Cx58通过MEF2B/Cx58轴与非小细胞肺癌的转移相关。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-25 DOI: 10.3724/abbs.2025049

Fen Tan, Juan Chen, Lunquan Sun, Lu Zhang, Rui Zhou

引用次数: 0

Corrigendum to: Melatonin protects TEGDMA-induced preodontoblast mitochondrial apoptosis via the JNK/MAPK signaling pathway. 褪黑素通过JNK/MAPK信号通路保护tegdma诱导的成牙前细胞线粒体凋亡。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-25 DOI: 10.3724/abbs.2025031

Qihao Yu, Ruize Hua, Bingyang Zhao, Dongchao Qiu, Chengfei Zhang, Shengbin Huang, Yihuai Pan

引用次数: 0

CRISPR-based shuttle cloning of 1,397 human genes into UAS vectors. 基于crispr的1397个人类基因穿梭克隆入UAS载体。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-25 DOI: 10.3724/abbs.2025050

Xuelian Liu, Hanqing Xi, Miao Dai, Xiaoxue Li, Wen Xue, Guang Chen, Jialong Yan, Si Xu, Guifang Ou, Si Luo, Yonghong Tang, Ping Wei, Jiwu Wang

引用次数: 0

Single-cell transcriptomic data reveal the cellular heterogeneity of glutamine metabolism in gastric premalignant lesions and early gastric cancer. 单细胞转录组学数据揭示了谷氨酰胺代谢在胃癌前病变和早期胃癌中的细胞异质性。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-23 DOI: 10.3724/abbs.2025061

Qingfeng Ni, Jiawei Yu, Yuanjie Niu, Zhenwei Han, Boyang Hu, Yang Wang, Jianwei Zhu

{"title":"Single-cell transcriptomic data reveal the cellular heterogeneity of glutamine metabolism in gastric premalignant lesions and early gastric cancer.","authors":"Qingfeng Ni, Jiawei Yu, Yuanjie Niu, Zhenwei Han, Boyang Hu, Yang Wang, Jianwei Zhu","doi":"10.3724/abbs.2025061","DOIUrl":"https://doi.org/10.3724/abbs.2025061","url":null,"abstract":"Glutamine metabolism is a hallmark of cancer metabolism. This study aims to perform a comprehensive and systematic single-cell profile of glutamine metabolism in premalignant and malignant gastric lesions. We use single-cell transcriptomics data from chronic atrophic gastritis (CAG) and early gastric cancer (EGC) lesions and investigate glutamine metabolism features at the single-cell level. Experiments are implemented to validate the expression and biological role of ERO1LB in gastric cancer (GC). A single-cell atlas based on 22511 cells from premalignant and early-malignant gastric lesions is established. Among these cells, epithelial cells constitute the dominant cell population in both CAG and EGC lesions. The activity of glutamine metabolism is higher in epithelial cells from EGC lesions than in those from CAG lesions. Among the epithelial cell subpopulations, glutamine metabolism is more active in the epithelial cell subpopulation cluster_4 in EGCs than in CAG lesions. As a key marker gene of this subpopulation, ERO1LB is experimentally proven to be overexpressed in human GC tissue lesions. In both in vitro and in vivo experiments, overexpression of ERO1LB in GC cells increases glutamine metabolism, facilitates cell growth and migration and prevents cell apoptosis, and vice versa. This study provides insight into the cellular heterogeneityof glutamine metabolism within the gastric mucosa in premalignant and malignant gastric lesions and identifies ERO1LB as a key orchestrator of glutamine metabolism, which may help to identify markers for GC prevention and contribute to our understanding of GC pathogenesis.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143956808","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

Long noncoding RNA UCA1 knockdown inhibits cisplatin-resistant cervical cancer tumorigenesis via the miR-195-5p/IKBKB axis. 长链非编码RNA UCA1敲低通过miR-195-5p/IKBKB轴抑制顺铂耐药宫颈癌的发生。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-22 DOI: 10.3724/abbs.2025032

Bi Wang, Ling Li, Zhengyu Wu, Xuanzhen Qian, Wenfeng Yu, Zhi Huang

{"title":"Long noncoding RNA UCA1 knockdown inhibits cisplatin-resistant cervical cancer tumorigenesis via the miR-195-5p/IKBKB axis.","authors":"Bi Wang, Ling Li, Zhengyu Wu, Xuanzhen Qian, Wenfeng Yu, Zhi Huang","doi":"10.3724/abbs.2025032","DOIUrl":"https://doi.org/10.3724/abbs.2025032","url":null,"abstract":"Cisplatin resistance is a major cause of poor prognosis in patients with cervical cancer. Dysregulation of long noncoding RNAs (lncRNAs) plays a key role in chemoresistance. Our results reveal that the lncRNA UCA1 is upregulated in cisplatin (DDP)-resistant cervical cancer tissues and HeLa cells. Mechanistically, the lncRNA UCA1 acts as a sponge for miR-195-5p, targeting IKBKB. UCA1 enhances proliferation, migration, and invasion while reducing apoptosis in DDP-resistant HeLa cells via the miR-195-5p/IKBKB axis. Additionally, UCA1 upregulates BNIP3Δex2 and p-p65 expressions and downregulates BNIP3 expression in DDP-resistant HeLa cells. Abnormal expressions of BNIP3Δex2 and BNIP3 significantly alter the malignant progression of HeLa/DPP cells. In vivo, UCA1 silencing inhibits growth, enhances apoptosis, and upregulates IKBKB, BNIP3Δex2, and p-p65 expressions while downregulating BNIP3 expression in subcutaneous xenografts in nude mice by targeting miR-195-5p. Overall, this study highlights a novel promising target for the treatment of DDP-resistant cervical cancer.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957407","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

D-mannose suppresses the angiogenesis and progression of colorectal cancer. d -甘露糖抑制结直肠癌的血管生成和进展。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-21 DOI: 10.3724/abbs.2025043

Yu Du, Xinchao Zhang, Yixin Xu, Yuefan Zhou, Yanping Xu

引用次数: 0

Integrated quantitative proteomics and phosphoproteomics analysis reveals USP46-POU4F1-HPSE signaling axis in the pathogenesis of Hirschsprung disease. 综合定量蛋白质组学和磷酸化蛋白质组学分析揭示了USP46-POU4F1-HPSE信号轴在巨结肠病发病机制中的作用。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-18 DOI: 10.3724/abbs.2025064

Guowei Li, Fengyin Sun, Jiawei Chen, Qiongqian Xu, Xintao Zhang, Luqiu Chen, Peimin Hou, Aiwu Li

{"title":"Integrated quantitative proteomics and phosphoproteomics analysis reveals USP46-POU4F1-HPSE signaling axis in the pathogenesis of Hirschsprung disease.","authors":"Guowei Li, Fengyin Sun, Jiawei Chen, Qiongqian Xu, Xintao Zhang, Luqiu Chen, Peimin Hou, Aiwu Li","doi":"10.3724/abbs.2025064","DOIUrl":"https://doi.org/10.3724/abbs.2025064","url":null,"abstract":"Hirschsprung's disease (HSCR) is a congenital disorder characterized by the absence of enteric ganglion cells in the distal colon, resulting in functional intestinal obstruction. While genetic mutations and microenvironmental imbalances have been implicated in HSCR, the underlying molecular mechanisms are not fully understood. This study uses integrated quantitative proteomics and phosphoproteomics analyses to characterize the differential protein profiles and phosphorylation modifications associated with HSCR. These findings reveal significant dysregulation of the extracellular matrix (ECM) remodelling pathway, suggesting its potential involvement in HSCR pathogenesis. Notably, the deubiquitinating enzyme USP46 is found to be significantly reduced in the aganglionic segments of HSCR patients. Through IP-MS, GST pull-down, and co-immunoprecipitation assays, it is demonstrated that USP46 interacts with the transcription factor POU4F1. Mechanistically, USP46 stabilizes POU4F1 via deubiquitination, increasing its binding to the heparanase (HPSE) promoter and increasing HPSE expression, which in turn promotes ECM remodelling and neural cell migration. The role of the USP46-POU4F1-HPSE signaling axis in HSCR pathogenesis is confirmed via chromatin immunoprecipitation-qPCR, luciferase reporter assays, and transwell migration assays. This study elucidates a novel regulatory mechanism linking USP46-mediated protein stabilization to ECM dynamics and neural cell migration, offering new insights into HSCR pathogenesis and potential therapeutic targets.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957917","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

Inhibition of HMOX1 alleviates diabetic cardiomyopathy by targeting ferroptosis. 抑制HMOX1通过靶向铁下垂缓解糖尿病性心肌病。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-16 DOI: 10.3724/abbs.2024232

Huiping Yang, Gongyi Xiao, Dinghui Wang, Tianhua Xiong, Jing Wang, Xiaodong Jing, Bingquan Xiong, Junmei Xie, Bin Liu, Qiang She

{"title":"Inhibition of HMOX1 alleviates diabetic cardiomyopathy by targeting ferroptosis.","authors":"Huiping Yang, Gongyi Xiao, Dinghui Wang, Tianhua Xiong, Jing Wang, Xiaodong Jing, Bingquan Xiong, Junmei Xie, Bin Liu, Qiang She","doi":"10.3724/abbs.2024232","DOIUrl":"https://doi.org/10.3724/abbs.2024232","url":null,"abstract":"Diabetic cardiomyopathy (DCM) is an important complication of chronic diabetes mellitus. However, its pathologic process and pathogenesis have not been fully elucidated. This study aims to investigate the role of ferroptosis in DCM and clarify the effect of heme oxygenase-1 (HMOX1) on DCM by targeting ferroptosis. In vivo, an animal model of DCM is established by subjecting mice to a high-fat diet (HFD) combined with low-dose streptozotocin (STZ) injection. We induce an in vitro DCM model by exposing H9C2 cells to high glucose and palmitic acid. Transcriptome sequencing reveals that the differentially expressed genes (DEGs) are enriched primarily in fatty acid metabolism and mitochondrial fatty acid β-oxidation, which are closely related to ferroptosis. The experimental results show that the diabetic microenvironment induces ferroptosis both in vivo and in vitro. Western blot analysis reveals the decreased expressions of the antioxidant proteins GPX4, SLC7A11 and ferritin in the DCM group. However, qPCR demonstrates the elevated expressions of the ferroptosis markers PTGS2 and ACSL4. Biochemical indicators further support the occurrence of ferroptosis, with increased levels of malondialdehyde (MDA) and lactate dehydrogenase (LDH), along with decreased level of glutathione (GSH). In vitro, intervention with high glucose and palmitic acid in H9C2 cells results in ferroptosis, which is reversed by ferrostatin-1 (Fer-1). Results show the elevated expression of HMOX1 in DCM. Moreover, knockdown of HMOX1 ameliorates ferroptosis, thereby alleviating diabetic cardiomyopathy by reducing cardiac fibrosis and improving cardiac function. Our study elucidates the role of HMXO1 in DCM pathogenesis and provides a potential therapeutic strategy for clinical treatment.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968559","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

Puerarin prevents cadmium-induced endoplasmic reticulum stress via SIRT1-dependent PERK-CHOP pathway in HepG2 cells. 葛根素通过sirt1依赖的PERK-CHOP途径阻止镉诱导的HepG2细胞内质网应激。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-11 DOI: 10.3724/abbs.2025039

Di Huang, Mengqi Qiu, Kuanhong Luo, Yanzhe Zhu, Siyu Zhang, Zhen He, Xiaobo Hu, Zhaohui Cao

{"title":"Puerarin prevents cadmium-induced endoplasmic reticulum stress via SIRT1-dependent PERK-CHOP pathway in HepG2 cells.","authors":"Di Huang, Mengqi Qiu, Kuanhong Luo, Yanzhe Zhu, Siyu Zhang, Zhen He, Xiaobo Hu, Zhaohui Cao","doi":"10.3724/abbs.2025039","DOIUrl":"https://doi.org/10.3724/abbs.2025039","url":null,"abstract":"Cadmium (Cd) is a high-risk heavy metal that induces oxidative stress, endoplasmic reticulum (ER) stress and inflammation, damaging organs such as the liver. Puerarin (PUE) has been shown to treat liver injury and especially prevent Cd-induced hepatic damage via its antioxidant activity. Sirtuin 1 (SIRT1), a histone deacetylase, is a key protector against various stress insults. However, its role in the protection of PUE against Cd-induced liver damage has not been clarified. Thus, this study is designed to elucidate the molecular mechanism in the human hepatoma cell line HepG2. The results first reveal that Cd-induced apoptosis is significantly restored by PUE pretreatment, as confirmed by the CCK-8, flow cytometric, Hoechst 33258 and TUNEL assays. Mechanistically, PUE significantly decreases ROS production and increases SOD levels in Cd-treated HepG2 cells. Moreover, PUE pretreatment alleviates ER stress by inhibiting the PERK-eIF2α-ATF4-CHOP axis and subsequently partially restores ER function as revealed by decreased Ca 2+ release from the ER. In addition, further study demonstrates that PUE upregulates SIRT1 expression, which suppresses the PERK signaling cascade and reduces CHOP levels. Collectively, our results first demonstrate that PUE protects HepG2 cells from Cd-induced apoptosis at least partially by inhibiting the PERK-eIF2α-ATF4-CHOP pathway in a SIRT1 expression-dependent manner. Puerarin appears to have great potential as a hepatoprotective agent.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958203","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

Withaferin A combined with ricolinostat: a potent synergistic therapy for cervical cancer through regulating p53 ubiquitination and acetylation. Withaferin A联合ricolinostat：通过调节p53泛素化和乙酰化治疗宫颈癌的有效协同疗法。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-04-10 DOI: 10.3724/abbs.2025048

Tian Chen, Yiting Xu, Kunming Yang, Yutong Du, Zhuan Zhu, Lingling Xu, Xinrong Wang, Yi Yin, Yu Hu, Chengcheng Wang, Ronggui Hu, Chuanyin Li

引用次数: 0