m6A­mediated LINC02038 inhibits colorectal cancer progression via regulation of the FAM172A/PI3K/AKT pathway via competitive binding with miR­552­5p.

ABSTRACT

Long noncoding RNAs (lncRNAs) are a type of regulatory molecule with potential roles in the development of several different malignancies. However, the underlying mechanisms of lncRNAs in colorectal cancer (CRC) are incompletely understood. The present study investigated the molecular mechanism of LINC02038 in CRC. LINC02038 expression was decreased in CRC tissues compared to the para­cancerous tissues and LINC02038 overexpression markedly reduced the proliferation, vitality, migration and invasive ability and greatly accelerated apoptosis of colorectal cancer cells. Bioinformatics examination indicated that LINC02038 may have targeted microRNA (miR)­552­5p. RNA immunoprecipitation and luciferase reporter assays showed that LINC02038 served as a sponge for miR­552­5p, hindering target gene FAM172A of miR­552­5p degradation. Moreover, methylated RNA immunoprecipitation (MeRIP)­qualitative PCR assays revealed that YTHDF2 could identify and regulate the METTL3­mediated LINC02038 N6­methyladenosine (m6A) modification and increase its degradation, thereby promoting CRC progression via the PI3K/AKT pathway. Based on the CRC clinical specimens, it was shown that LINC02038 was negatively associated with lymphatic metastasis and distant metastasis. These results revealed that m6A/LINC02038/miR­552­5p/FAM172A may be a novel anti­tumor axis and LINC02038 may serve as a biomarker and treatment option for colorectal cancer.