CircARID1A promotes gastric cancer progression by targeting the miR-147a/SNAI2 signaling axis
TL;DR
In vivo, knockdown of circARID1A inhibits tumor growth in subcutaneous xenograft models and promotes GC cell proliferation, migration, and invasion by regulating the miR-147a/SNAI2 axis.
Abstract
ABSTRACT Due to the late stage at which most gastric cancer patients are diagnosed, the prognosis is often poor. Current treatments have limited efficacy for advanced cases. This study delves into the involvement of circARID1A and the mechanisms behind its role in gastric cancer progression. GES-1 cell line and GC cell lines HGC-27, AGS, MKN45, and SNU-16 were cultured and subjected to various assays. RNA interference and overexpression techniques were used to modulate circARID1A and miR-147a levels in vitro, while xenograft tumor models in BALB/c nude mice were used to assess tumor growth in vivo. Cellular growth, migration, and invasion were assessed using CCK8, colony formation, and Transwell assays. Dual-luciferase reporter assays, qPCR and Western blot were utilized to investigate the interactions between circARID1A, miR-147a, and SNAI2. CircARID1A promotes GC cell proliferation, migration, and invasion by regulating the miR-147a/SNAI2 axis. In vivo, knockdown of circARID1A inhibits tumor growth in subcutaneous xenograft models.