Skip to main content
. 2019 Jan 31;19(4):2489–2496. doi: 10.3892/mmr.2019.9916

Figure 3.

Figure 3.

JMJD2A knockdown induces miR-491-5p expression in cervical cancer cells. (A) Western blotting demonstrates that JMJD2A knockdown induced the expression of pro-apoptotic proteins (active caspase-3, Bax and p21) and inhibited the expression of the anti-apoptotic protein Bcl-2 in HeLa cells. (B) miR-491-5p mRNA levels are downregulated in HeLa, CaSki, C-4-I, SiHa and C-33 A human cervical cancer cell lines. ***P<0.001 vs. normal. (C) The miR-491-5p and JMJD2A levels were negatively correlated in the human cervical cancer specimens (n=38). (D) JMJD2A knockdown significantly increased the level of miR-491-5p, and JMJD2A overexpression significantly decreased the level of miR-491-5p in cervical cancer cell lines. ***P<0.001 vs. Ad-NC; ###P<0.001 vs. sh-NC. (E) Kaplan-Meier survival rate analysis demonstrates that the overall survival rate is poor for cervical cancer patients with low miR-491-5p expression. The mean miR-491-5p level of the cervical cancer tissues was evaluated using reverse transcription-quantitative polymerase chain reaction. The cases whose miR-491-5p level was lower than the mean miR-491-5p level were enrolled to the miR-491-5p low group, while the others were enrolled in the miR-491-5p high group. (F) miR-491-5p levels following the transfection of LNA-miR-491-5p and LNA-NC into sh-JMJD2A and sh-NC cells. ***P<0.001 vs. LNA-NC + Sh-NC; ###P<0.001 vs. LNA-miR-491-5p + Sh-JMJD2A. JMJD2A, jumonji domain containing 2A; sh, short hairpin; Ad, adenovirus; NC, negative control; Bax, Bcl-2-like protein 4; Bcl-2, B-cell lymphoma.