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. 2019 Aug 19;12:6623–6638. doi: 10.2147/OTT.S196630

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© 2019 Wu et al.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

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BMI1 was a direct target of miR-139-5p. (A) The relationship of miR-139-5p and BMI1 was predicted by starbase. (B and C) WT-BMI1 or MUT-BMI1 was cotransfected into Hep3B (B) and HepG2 (C) cells with miR-139-3p or their negative controls. (D and E) WT-BMI1 or MUT-BMI1 was cotransfected into Hep3B (D) and HepG2 (E) cells with miR-139-3p inhibitor or their negative controls. (F) BMI1 expression in HCC tissues. (G) BMI1 expression in LC-02, Hep3B, and HepG2 cells. (H) BMI1 expression under the condition of miR-139-5p overexpression in Hep3B and HepG2 cells. (I) BMI1 expression under the condition of SNHG3 overexpression in Hep3B and HepG2 cells. *P<0.05.

Abbreviations: HCC, hepatocellular carcinoma; SNHG3, small nucleolar RNA host gene 3.