Published online Sep 15, 2023. doi: 10.4251/wjgo.v15.i9.1556
Peer-review started: May 5, 2023
First decision: July 9, 2023
Revised: July 21, 2023
Accepted: August 18, 2023
Article in press: August 18, 2023
Published online: September 15, 2023
Processing time: 131 Days and 8.7 Hours
Colorectal cancer is the second most common cause of cancer death, however, the molecular mechanisms of tumorigenesis and development of colorectal cancer are far from being elucidated.
MicroRNAs play important roles in gene regulation and modulate numerous physical and pathological processes. The motivation of this study is to reveal the role of microRNA-363-3p (miR-363-3p) in the development of colorectal cancer and the underlying mechanisms.
Compare the expression of miR-363-3p between colorectal cancer tissues and adjacent normal tissues; clarify the role of miR-363-3p in clonogenic survival, migration, and proliferation of colorectal cancer cells; identify the direct target of miR-363-3p in colorectal cancer cells.
Real-time polymerase chain reaction was performed to detect miRNA expression. PITA 6 was utilized to predict the targets of miR-363-3p. Dual-luciferase reporter system was used to validate the target of miR-363-3p. Plate colony formation and wound-healing assays were performed to evaluate cancer cells’ clonogenic survival and migration ability, respectively. Cell proliferation was examined by cell counting kit-8 assay. Immunohistochemical staining was used to determine the expression level of interferon-induced transmembrane protein 1 (IFITM1).
MiR-363-3p was decreased in colorectal cancer tissues. IFITM1 was characterized as a direct target of miR-363-3p.
MiR-363-3p inhibits clonogenic survival, proliferation, and migration of colorectal cancer cells via targeting IFITM1.
MiR-363-3p/IFITM1 axis may represent a therapeutic target in colorectal cancer.