RT Journal Article
SR Electronic
T1 <em>MiR-532-3p</em> inhibited the methylation of <em>SOCS2</em> to suppress the progression of PC by targeting <em>DNMT3A</em>
JF Life Science Alliance
JO Life Sci. Alliance
FD Life Science Alliance LLC
SP e202201703
DO 10.26508/lsa.202201703
VO 6
IS 5
A1 Wang, Kaiqiong
A1 Gong, Dongwei
A1 Qiao, Xin
A1 Zheng, Jinfang
YR 2023
UL https://www.life-science-alliance.org/content/6/5/e202201703.abstract
AB Pancreatic cancer (PC) is one of the deadliest malignancies, with poor diagnosis and prognosis. miR-532-3p has been reported to be a tumor suppressor in various cancers, whereas the mechanism of miR-532-3p in the progression of PC remains poorly understood. In this study, it was found that miR-532-3p and SOCS2 were down-regulated, whereas DNMT3A was up-regulated in PC. Knockdown of DNMT3A or overexpression of miR-532-3p suppressed PC cell proliferation, invasion, and migration, as well as tumor formation in nude mice. DNMT3A induced the methylation of SOCS2 promoter. SOCS2 knockdown reversed the inhibiting effect of DNMT3A silencing on PC cell growth. miR-532-3p directly bound to DNMT3A and negatively regulated its expression while up-regulating SOCS2 levels. DNMT3A overexpression reversed the inhibiting effect of miR-532-3p overexpression on PC cell growth. In conclusion, the overexpression of miR-532-3p could suppress proliferation, invasion, and migration of PC cells, as well as tumor formation in nude mice through inhibiting the methylation of SOCS2 by targeting DNMT3A.