Open AccessMicroRNA‑1307‑3p accelerates the progression of colorectal cancer via regulation of TUSC5
Author(s) -
Yue Na,
Ming Ye,
Ran Zhang,
Miao Wang
Publication year - 2020
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2020.8814
Subject(s) - oncogene , microrna , gene knockdown , colorectal cancer , cancer research , cell growth , cell cycle , biology , reporter gene , luciferase , downregulation and upregulation , cell culture , cell , suppressor , molecular medicine , cancer , transfection , gene expression , gene , genetics
The aim of the present study was to explore the roles of microRNA-1307-3p (miR-1307-3p) in colorectal cancer (CRC). Firstly, the expression level of miR-1307-3p in CRC cells was measured using reverse transcription-quantitative PCR. Subsequently, Cell Counting Kit-8 and Transwell invasion assays were performed to evaluate the effects of miR-1307-3p on CRC cell proliferation and invasion, respectively. Bioinformatics tools and dual luciferase reporter assays were used to validate the targets of miR-1307-3p. Rescue experiments were performed to confirm tumor suppressor candidate 5 (TUSC5) as a functional target of miR-1307-3p. miR-1307-3p levels were revealed to be upregulated in CRC cells when compared with the normal human epithelial cell line. Knockdown of miR-1307-3p inhibited CRC cell growth and invasiveness. Bioinformatics analysis and dual-luciferase activity reporter assays demonstrated that miR-1307-3p binds the 3'-untranslated region of TUSC5. Finally, rescue experiments validated that miR-1307-3p was able to regulate CRC cell behaviors via regulating TUSC5 expression. Together, the current results indicate that miR-1307-3p functions as an oncogenic miRNA via targeting TUSC5 in CRC.