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
(lnc
RNA
)
UCA
1 has been shown to promote the proliferation and invasion of cervical cancer cells through regulating miR‐206 expression, but the involvement of
UCA
1 in regulating the stemness and epithelial–mesenchymal transition (
EMT
) of glioma cells is unknown. Here, we report that the expression of
UCA
1 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 lnc
RNA UCA
1 attenuated these two processes and their enhancement by
TGF
‐β. Mechanistically, knockdown of
UCA
1 decreased Slug expression by acting as a competitive endogenous
RNA
(ce
RNA
) 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
UCA
1 knockdown on Slug expression, and
UCA
1 colocalized with miR‐1 and miR‐203a in glioma tissues. Notably, ectopic expression of Slug rescued the attenuation of
UCA
1 knockdown on
EMT
and the stemness of glioma cells. These results indicate that
UCA
1 may act as a ce
RNA
to promote Slug expression, which underlies
TGF
‐β‐induced
EMT
and stemness of glioma cells.
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