Upregulation of miRNA-10a-5p promotes tumor progression in cervical cancer by suppressing UBE2I signaling

Figures & data

Figure 1. MiR-10a-5p targets UBE2I in CC cells. (A) Binding sites between UBE2I and miR-10a-5p. (B) Luciferase activity in UBE2I WT or Mut transfected Hela cells with or without miR-10a-5p upregulation. (C) UBE2I abundance in CC tissues. (D) The abundance of UBE2I in CC cells. (E) The UBE2I mRNA abundance in Hela cells transfecting the miR-10a-5p mimic. (F) The UBE2I protein abundance in Hela cells transfecting the miR-10a-5p mimic.

Figure 2. UBE2I suppression counteracts the influence of miR‑10a‑5p downregulation on CC cell growth. (A) The efficiency of UBE2I knockdown. (B) Cell viability was measured after co-transfecting cells with miR‑10a‑5p inhibitors and sh-UBE2I. (C) Hela cell proliferation after UBE2I knockdown was analyzed. (D) The proportion of apoptotic Hela cells after UBE2I knockdown. (E) The protein abundance of Bax, caspase-3 and -9, as well as Bcl-2 in Hela cells transfecting miR‑10a‑5p inhibitors and sh-UBE2I.

Figure 3. Inhibition of UBE2I counteracts the influence of miR‑10a‑5p downregulation on CC cell metastasis. (A) Hela cell migration after the knockdown of UBE2I was determined. (B) The metastasis compacity of Hela cells after UBE2I inhibition. (C) Western blot analyzed pro-invasive factors MMP2 and MMP9 abundance after co-transfecting cells with miR‑10a‑5p inhibitor and sh-UBE2I.

Data availability statement

All data generated or analyzed during this study are included in this published article.