MicroRNA-23a promotes colorectal cancer cell migration and proliferation by targeting at MARK1

• Published in: Acta biochimica et biophysica Sinica Vol. 51; no. 7; pp. 661 - 668
• Main Authors: Tang, Xiaoli, Yang, Meiyuan, Wang, Zheng, Wu, Xiaoqing, Wang, Daorong
• Format: Journal Article
• Language: English
• Published: China Oxford University Press 10.07.2019
• Subjects: 3' Untranslated Regions - genetics; Base Sequence; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; Colorectal Neoplasms - genetics; Colorectal Neoplasms - metabolism; Colorectal Neoplasms - pathology; Female; Gene Expression Regulation, Neoplastic; HCT116 Cells; Humans; Male; MicroRNAs - genetics; Middle Aged; Protein-Serine-Threonine Kinases - genetics; Protein-Serine-Threonine Kinases - metabolism; Sequence Homology, Nucleic Acid; MARK1 protein; colorectal neoplasms, microRNA-23a
• ISSN: 1672-9145; 1745-7270
• DOI: 10.1093/abbs/gmz047

Abstract The functional role of microRNA-23a in tumorigenesis has been investigated; however, the exact mechanism of microRNA-23a (miR-23a) in colorectal cancer development has not been fully explored. In the present study, we aimed to investigate the molecular functional role of miR-23a in colorectal carcinogenesis. Quantitative real-time polymerase chain reaction was conducted to investigate the expression level of miR-23a in tissue samples and cell lines (HCT116 and SW480). CCK-8, colony formation and Transwell assay were used to explore the role of miR-23a in cell proliferation and migration. Dual luciferase reporter assay was used to identify the direct binding of miR-23a with its target, MARK1. Western blot analysis was used to analyze the expression level of MARK1, as well as a confirmed miR-23a target gene, MTSS1, in miR-23a-mimic and miR-23a-inhibit groups. Rescue experiments were conducted by overexpression of MARK1 in miR-23a-mimic-transfected cell lines. The results showed that miR-23a was highly expressed in colorectal cancer tissue and cell lines. MiR-23a could promote proliferation and migration of colorectal cancer cell lines. MARK1 was a direct target of miR-23a and the expression level of MARK1 was down-regulated in miR-23a-mimic-transfected cell lines but up-regulated in miR-23a-inhibit-transfected cells. Overexpression of MARK1 could partly reverse the cancer-promoting function of miR-23a. Our results suggested that miR-23a promotes colorectal cancer cell proliferation and migration by mediating the expression of MARK1. MiR-23a may be a potential therapeutic target for colorectal cancer treatment.