LncRNA HCG11 mediated by METTL14 inhibits the growth of lung adenocarcinoma via IGF2BP2/LATS1

Abstract

Lung adenocarcinoma (LUAD) is a common malignancy the pathogenesis of which is terribly complicated and remains largely unclear. Long non-coding RNAs (lncRNAs) are a group of endogenous RNA molecules that are involved in various malignant processes. In this study, we explored the roles of lncRNA Human leukocyte antigen complex group 11 (HCG11) in LUAD. Our data revealed that lncRNA HCG11 expression was downregulated in LUAD, which was modulated by the hypermethylation of HCG11 promoter and Methyltransferase Like 14 (METTL14) mediated N6-methyladenosine (m6A) modification. The m6A modification of HCG11 promoted its nuclear exportation and binding by Insulin Like Growth Factor 2 MRNA Binding Protein 2 (IGF2BP2), resulting in increased stability. HCG11 could recruit IGF2BP2 to target Large Tumor Suppressor Kinase 1 (LATS1) mRNA to enhance the stability and promote the expression of LATS1. HCG11 served as a tumor suppressor to restrain tumor growth in LUAD by regulating LATS1. In summary, this study demonstrated that HCG11 mediated by METTL14 inhibited the growth of lung adenocarcinoma via IGF2BP2/LATS1.