Long noncoding RNA Meg3 sponges miR-708 to inhibit intestinal tumorigenesis via SOCS3-repressed cancer stem cells growth

MEG3 Competing Endogenous RNA
DOI: 10.1038/s41419-021-04470-5 Publication Date: 2021-12-21T14:05:37Z
ABSTRACT
Abstract Background Colorectal cancer (CRC) remains the most common gastrointestinal and a leading cause of deaths worldwide, with showing pathologies indicating malignant transformation early stage intestinal stem cells. The long non-coding RNA Meg3 , which functions as tumor suppressor, has been reported to be abnormal in multiple tumorigenesis events; however, underlying mechanism by contributes proliferation colonic cells unclear. Methods We analyzed expression levels miR-708 SOCS3 samples from Apc loss-of-function ( min ) mice patients CRC, particularly crypt AMO/DSS-induced model (in vivo) organoid culture system vitro) were used explore effect / /SOCS3 axis on colon. In vitro, we performed RNApull-down, immunoprecipitation, luciferase reporter assays using DLD1 RKO cell lines. Findings signaling plays critical role CRC development. Our data showed negatively correlate both clinical mouse model, indicated that acts competitive endogenous (ceRNA) . Then, served an oncogene, inducing neoplasia cultured organoids. Put together, appears promote targeting SOCS3/STAT3 signaling. Interpretation These revealed sponges inhibit development via SOCS3-mediated repression provides potential targets for diagnosis treatment CRC.
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