MiR-532-3pinhibited the methylation ofSOCS2to suppress the progression of PC by targetingDNMT3A

Abstract

Pancreatic cancer (PC) is one of the deadliest malignancies, with poor diagnosis and prognosis.miR-532-3phas been reported to be a tumor suppressor in various cancers, whereas the mechanism ofmiR-532-3pin the progression of PC remains poorly understood. In this study, it was found thatmiR-532-3pandSOCS2were down-regulated, whereasDNMT3Awas up-regulated in PC. Knockdown ofDNMT3Aor overexpression ofmiR-532-3psuppressed PC cell proliferation, invasion, and migration, as well as tumor formation in nude mice. DNMT3A induced the methylation ofSOCS2promoter.SOCS2knockdown reversed the inhibiting effect ofDNMT3Asilencing on PC cell growth.miR-532-3pdirectly bound toDNMT3Aand negatively regulated its expression while up-regulatingSOCS2levels.DNMT3Aoverexpression reversed the inhibiting effect ofmiR-532-3poverexpression on PC cell growth. In conclusion, the overexpression ofmiR-532-3pcould suppress proliferation, invasion, and migration of PC cells, as well as tumor formation in nude mice through inhibiting the methylation ofSOCS2by targetingDNMT3A.