Published online Mar 7, 2020. doi: 10.3748/wjg.v26.i9.933
Peer-review started: December 5, 2019
First decision: December 30, 2019
Revised: January 8, 2020
Accepted: January 19, 2020
Article in press: January 19, 2020
Published online: March 7, 2020
As the most common biliary malignancy, GC is an elderly-biased disease. Although extensive studies have elucidated the molecular mechanism of miR-182 and RECK in various cancers, the specific roles of exosomal miR-182 and RECK in GC remain poorly understood.
The expression of miR-182 and exosomal miR-182 was increased in gallbladder cancer, while RECK decreased. Targetscan7.2 predicted RECK could bind with miR-182 via 3’UTR. RECK was negatively correlated with miR-182.
This study was set out to explore the relationship between exosomal miR-182/RECK and metastasis of GC.
Paired GC and adjacent normal tissues were collected from 78 patients. qPCR was employed to detect miR-182 and exosomal miR-182 expression, and Western blot was adopted to determine RECK expression. In addition, the effect of exosomal miR-182/RECK on the biological function of human GC cells were observed. Moreover, double luciferase reporter gene assay was applied to validate the targeting relationship between miR-182 and RECK.
Compared with normal gallbladder epithelial cells, miR-182 was highly expressed in GC cells, while RECK was lowly expressed. Exosomal miR-182 could be absorbed and transferred by cells. Exosomal miR-182 inhibited RECK expression and promoted migration and invasion of GC cells.
Exosomal miR-182 can significantly promote the migration and invasion of GC cells by inhibiting RECK, and thus miR-182 can be used as a therapeutic target for GC.
The signaling pathways implicated in miR-182/RECK should be explored in future experimental design to supplement the oncogenic network of exosomal miR-182. The clinical value of exosomal miR-182 in GC remains to be discussed.