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已发表论文
环状 RNA DENND4C 通过 miR-26a-5p/HSPA8 轴调控乳腺癌细胞的恶性行为
Authors Guo M, Chang Y, Dai Y, Liu X, Shi S, Li J, Liu W, Han J
Received 21 May 2025
Accepted for publication 30 October 2025
Published 2 December 2025 Volume 2025:17 Pages 1145—1157
DOI https://doi.org/10.2147/BCTT.S541889
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Pranela Rameshwar
MeiYan Guo,1,* Yan Chang,1,* YuNa Dai,1 Xia Liu,2 SuFang Shi,1 JuMei Li,1 WeiGuang Liu,3 JianJun Han1
1Department of Breast Surgery, Affiliated Hospital of Hebei Engineering University, Handan City, Hebei Province, 056002, People’s Republic of China; 2Department of Health Examination, Affiliated Hospital of Hebei Engineering University, Handan City, Hebei Province, 056002, People’s Republic of China; 3Department of Breast Surgery, Yangzhou Maternal and Child Health Hospital, Yangzhou City, Jiangsu Province, 225007, People’s Republic of China
*These authors contributed equally to this work
Correspondence: JianJun Han, Department of Breast Surgery, Affiliated Hospital of Hebei Engineering University, No. 81, Congtai Road, Congtai District, Handan City, Hebei Province, 056002, People’s Republic of China, Email hanjianjunHJJ@outlook.com
Objective: At present, the potential functions of most circRNAs in breast cancer (BC) have not been fully elucidated. The investigatory research planned to study biological function of circDENND4C in BC and reveal its downstream molecular mechanism.
Methods: A total of fifty pairs of BC tissue and their corresponding normal tissue were obtained. circDENND4C/miR-26a-5p/Human 71 kDa heat shock cognate protein (HSPA8) were assessed through RT-qPCR or Western blot. After transfecting the relevant plasmids, MKN-45 cell proliferation, cell cycle, invasion, and migration were assessed through MTT and colony formation assays, flow cytometry, and Transwell tests. Bioinformatics analysis, RIP and dual luciferase reporting experiments verified the interaction between circDENND4C, miR-26a-5p, and HSPA8.
Results: Increased circDENND4C was found in BC and was related to a poor prognosis in BC patients. HSPA8 was upregulated and miR-26a-5p was downregulated in BC. Functionally, silencing circDENND4C prevented cells from proliferation, invasion, and migration, and induced cell cycle arrest at G0/G1 phase. circDENND4C overexpression had the opposite effect. The effects of circDENND4C overexpression or knockdown in BC cells were counteracted by overexpressing miR-26a-5p or HSPA8, respectively. circDENND4C mediated HSPA8 expression by competitively adsorbing miR-26a-5p.
Conclusion: circDENND4C absorbs miR-26a-5p to target HSPA8, thereby promoting BC progression, which provides a new insight into the mechanism of BC.
Keywords: circDENND4C, breast cancer, miR-26a-5p, HSPA8
1Department of Breast Surgery, Affiliated Hospital of Hebei Engineering University, Handan City, Hebei Province, 056002, People’s Republic of China; 2Department of Health Examination, Affiliated Hospital of Hebei Engineering University, Handan City, Hebei Province, 056002, People’s Republic of China; 3Department of Breast Surgery, Yangzhou Maternal and Child Health Hospital, Yangzhou City, Jiangsu Province, 225007, People’s Republic of China
*These authors contributed equally to this work
Correspondence: JianJun Han, Department of Breast Surgery, Affiliated Hospital of Hebei Engineering University, No. 81, Congtai Road, Congtai District, Handan City, Hebei Province, 056002, People’s Republic of China, Email hanjianjunHJJ@outlook.com
Objective: At present, the potential functions of most circRNAs in breast cancer (BC) have not been fully elucidated. The investigatory research planned to study biological function of circDENND4C in BC and reveal its downstream molecular mechanism.
Methods: A total of fifty pairs of BC tissue and their corresponding normal tissue were obtained. circDENND4C/miR-26a-5p/Human 71 kDa heat shock cognate protein (HSPA8) were assessed through RT-qPCR or Western blot. After transfecting the relevant plasmids, MKN-45 cell proliferation, cell cycle, invasion, and migration were assessed through MTT and colony formation assays, flow cytometry, and Transwell tests. Bioinformatics analysis, RIP and dual luciferase reporting experiments verified the interaction between circDENND4C, miR-26a-5p, and HSPA8.
Results: Increased circDENND4C was found in BC and was related to a poor prognosis in BC patients. HSPA8 was upregulated and miR-26a-5p was downregulated in BC. Functionally, silencing circDENND4C prevented cells from proliferation, invasion, and migration, and induced cell cycle arrest at G0/G1 phase. circDENND4C overexpression had the opposite effect. The effects of circDENND4C overexpression or knockdown in BC cells were counteracted by overexpressing miR-26a-5p or HSPA8, respectively. circDENND4C mediated HSPA8 expression by competitively adsorbing miR-26a-5p.
Conclusion: circDENND4C absorbs miR-26a-5p to target HSPA8, thereby promoting BC progression, which provides a new insight into the mechanism of BC.
Keywords: circDENND4C, breast cancer, miR-26a-5p, HSPA8