LncRNA UCA1 is necessary for TGF-β-induced epithelial-mesenchymal transition and stemness via acting as a ceRNA for Slug in glioma cells.

Abstract

The 5‐year survival rate of patients with glioma is < 5%, and therefore there is an urgent need to find novel potential targets for facilitating its diagnosis and treatment. The long non‐coding RNA (lncRNA) UCA1 has been shown to promote the proliferation and invasion of cervical cancer cells through regulating miR‐206 expression, but the involvement of UCA1 in regulating the stemness and epithelial–mesenchymal transition (EMT) of glioma cells is unknown. Here, we report that the expression of UCA1 is significantly increased by transforming growth factor‐β (TGF‐β) treatment in glioma cells and is greater in glioma tissues than in normal adjacent tissues. Additionally, TGF‐β induced EMT and the stemness of glioma cells, whereas knockdown of lncRNA UCA1 attenuated these two processes and their enhancement by TGF‐β. Mechanistically, knockdown of UCA1 decreased Slug expression by acting as a competitive endogenous RNA (ceRNA) through competitive binding with miR‐1 and miR‐203a; this effect was further evidenced by the fact that transfection with miR‐1 or miR‐203a inhibitors abrogated the effects of UCA1 knockdown on Slug expression, and UCA1 colocalized with miR‐1 and miR‐203a in glioma tissues. Notably, ectopic expression of Slug rescued the attenuation of UCA1 knockdown on EMT and the stemness of glioma cells. These results indicate that UCA1 may act as a ceRNA to promote Slug expression, which underlies TGF‐β‐induced EMT and stemness of glioma cells.