Long non-coding RNA MBNL1-AS1 regulates proliferation, migration, and invasion of cancer stem cells in colon cancer by interacting with MYL9 via sponging microRNA-412-3p

Background/aims: Colon cancer is a common cancer that is a threat to human health. Some long non-coding RNAs (lncRNAs) have been observed to exert roles in colon cancer. Here, the current study is aimed to explore the potential mechanism of lncRNA MBNL1 antisense RNA 1 (MBNL1-AS1) in progression of colon cancer and the associated mechanisms.

Methods: Microarray analysis was performed to screen differentially expressed lncRNA and genes associated with colon cancer and its potential mechanism. The functional role of MBNL1-AS1 in colon cancer was analyzed, followed identification of the interaction among MBNL1-AS1, microRNA-412-3p (miR-412-3p), and MYL9. Subsequently, CSC viability, migration, invasion, and apoptosis were detected though a series of in vitro experiments. At last, in vivo experiments were performed to assess tumor formation of colon CSCs.

Results: MBNL1-AS1 and MYL9 were poorly expressed in colon cancer. MBNL1-AS1 could competitively bind to miR-412-3p so as to promote MYL9 expression. Enhancement of MBNL1-AS1 or inhibition of miR-412-3p was shown to decrease CSC proliferation, migration, and invasion but promote apoptosis. Moreover, MBNL1-AS1 reversed the CSC-like properties as well as xenograft tumor formation in vivo induced by miR-412-3p.

Conclusion: Collectively, the present study suggests an inhibitory role of MBNL1-AS1 in colon cancer by upregulating miR-412-3p-targeted MYL9. Thus, this study provides an enhanced understanding of MBNL1-AS1 along with miR-412-3p and MYL9 as therapeutic targets for colon cancer.