LncRNA ELFN1-AS1 enhances the progression of colon cancer by targeting miR-4270 to upregulate AURKB.

Abstract

The oncogenic role of lncRNA ELFN1-AS1 has been described in different cancers, including colon cancer (CC). However, how ELFN1-AS1 regulates CC malignancy remains unclear. In this study, ELFN1-AS1, AURKB, and miR-4270 expression levels in CC cells and tissues were determined using RT-qPCR and western blotting. CCK-8 and wound healing assays were also performed to analyze alterations in CC cell proliferation and migration. The expression of apoptosis-related proteins (Bax and Bcl-2) was determined via western blot analysis. RNA immunoprecipitation (RIP) assays coupled with luciferase reporter assays were employed to verify the relationship between miR-4270, ELFN1-AS1, and AURKB. An in vivo assay was performed using xenograft tumors in mice to detect the change of tumor growth. It was found that AURKB and ELFN1-AS1 expression was upregulated, whereas miR-4270 was downregulated in CC cells and tissues. ELFN1-AS1 silencing exhibited anti-proliferative, anti-migratory, and pro-apoptotic effects in CC cells. The tumor-suppressive effect of ELFN1-AS1 silencing was verified using in vivo assays. MiR-4270 was predicted to be a target of ELFN1-AS1 and AURKB as a target of miR-4270. Their interactions were further elucidated using luciferase reporter and RNA RIP assays. More importantly, treatment with a miR-4270 inhibitor not only rescued the tumor-suppressing effect of ELFN1-AS1 silencing but also abrogated the tumor suppressor functions of AURKB silencing in CC cells. Taken together, the ELFN1-AS1/miR-4270/AURKB axis facilitates CC tumorigenesis; therefore, targeting this axis might be a promising intervention in preventing CC progression.