Published online Jan 21, 2021. doi: 10.3748/wjg.v27.i3.240
Peer-review started: October 30, 2020
First decision: November 30, 2020
Revised: December 4, 2020
Accepted: December 16, 2020
Article in press: December 16, 2020
Published online: January 21, 2021
Esophageal cancer is one of the most malignant tumors in the digestive system and exploring the underlying mechanism is a key issue that needs to be addressed. Circular RNA AKT3 (circAKT3) is a novel noncoding RNA participating in the development and progression of multiple tumors.
To identify biomarkers for the diagnosis and treatment of esophageal cancer.
To explore the mechanism of the role of circAKT3 in the development of esophageal cancer.
Cell Counting Kit-8, wound healing assay, Transwell assay, and fluorescence analysis were used to evaluate the circAKT3 effect on proliferation, migration, invasion, and apoptosis of esophageal cancer cells.
In vitro assays results revealed that proliferative, migratory, and invasive capacities of esophageal cancer cells were significantly enhanced by circAKT3 overexpression. miR-17-5p was screened as the target of circAKT3, and miR-17-5p antagonized the effects of circAKT3 on esophageal cancer cells. Moreover, we identified RHOC and STAT3 as the direct target molecules of miR-17-5p, and circAKT3 facilitated expression of RHOC and STAT3 by inhibiting miR-17-5p. In vivo assays showed circAKT3 knockdown inhibited growth of esophageal cancer.
CircAKT3 enhanced proliferative, migratory, and invasive capacities of esophageal cancer cells by sponging miR-17-5p to exert protumor effects, and downregulation of circAKT3 inhibited xenograft tumor growth of esophageal cancer in vivo, providing a potential target for better understanding the underlying mechanism of esophageal cancer.
The role of circAKT3 in other tumors may be uncovered in the future, and its application in anticancer therapy will be promoted.