MiR-16-5p suppresses breast cancer proliferation by targeting ANLN
Ziming Wang,
Siyuan Hu,
Xinyang Li,
Zhiwei Liu,
Danyang Han,
Yukun Wang,
Limin Wei,
Guangping Zhang,
Xinshuai Wang
Affiliations
Ziming Wang
Henan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and Technology
Siyuan Hu
Zhoukou first people’s Hospital
Xinyang Li
Henan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and Technology
Zhiwei Liu
Henan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and Technology
Danyang Han
Henan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and Technology
Yukun Wang
Henan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and Technology
Limin Wei
Henan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and Technology
Guangping Zhang
Henan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and Technology
Xinshuai Wang
Henan Key Laboratory of Cancer Epigenetics; Cancer hospital, The First Affiliated Hospital, College of Clinical Medicine, Medical College of Henan University of Science and Technology
Abstract Background In recent years, gene expression-based analysis has been used for disease biomarker discovery, providing ways for better diagnosis, leading to improvement of clinical treatment efficacy. This study aimed to explore the role of miR-16-5p and ANLN in breast cancer (BC). Methods Cohort datasets of BC were obtained from the Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) and analyzed by bioinformatics tools. qRT-PCR and western blotting were applied to validate ANLN and its protein expression. A dual-luciferase reporter assay was used to prove the regulatory relationship of miR-16-5p and ANLN. Finally, MTT, wound healing, Transwell invasion and flow cytometry analyses of the cell cycle and apoptosis were performed to assess cell proliferation, migration, invasion, cell cycle and apoptosis, respectively. Results A total of 195 differentially expressed genes (DEGs) and 50 overlapping microRNAs (miRNAs) were identified. Among these DEGs and miRNAs, ANLN, associated with poor overall survival in BC, overlapped in the GSE29431, GSE42568, TCGA and GEPIA2 databases. Moreover, ANLN was highly expressed, while miR-16-5p was lower in BC cells than in breast epithelial cells. Then, we confirmed that ANLN was directly targeted by miR-16-5p in BC cells. Over-expression of miR-16-5p and knock-down of ANLN remarkably inhibited cell proliferation and migration as well as cell invasion, arrested the cells in G2/M phase and induced apoptosis in BC cells. Conclusions These findings suggest that miR-16-5p restrains proliferation, migration and invasion while affecting cell cycle and promotes apoptosis by regulating ANLN, thereby providing novel candidate biomarkers for the diagnosis and treatment of BC.
