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. 2020 Nov 19;45(1):95–106. doi: 10.3892/or.2020.7862

Figure 4.

Figure 4.

miR-3184-5p attenuates cervical cancer cell viability and invasion by targeting ERBB2. (A) Putative binding location for miR-3184-5p on ERBB2 3′-UTR via TargetScan analysis. (B) miR-3184-5p expression in HeLa and SiHa cervical cancer cell lines compared with in the non-cancerous human H8 cervical epithelial cell line assessed via RT-qPCR. U6 was used as the housekeeping control. **P<0.01 vs. H8; ††P<0.01 vs. SiHa. Luciferase reporter assay of ERBB2-3′-UTRWT or ERBB2-3′-UTRMU in (C) HeLa or (D) SiHa cells transfected with miR-3184-5p mimic or inhibitor, respectively. **P<0.01 vs. Ctrl mimic or Ctrl inhib. WB of (E) HeLa and (F) SiHa cells transfected with miR-3184-5p mimic or inhibitor, respectively. (G) Invasion of transfected HeLa cells assessed via Transwell assay. (H) Cellular viability of transfected HeLa cells quantified using Cell Counting Kit-8. (I) Sphere-formation of transfected HeLa cells. Data are expressed as the mean ± SEM (n=3). **P<0.01 vs. Ctrl vec; ††P<0.01 vs. miR-3184-5p mimic. Data were analyzed via one-way ANOVA. UTR, untranslated region; WT, wild-type; MU, mutant; Ctrl, control; inhib, inhibitor; WB, western blotting; RT-qPCR, reverse transcription-quantitative PCR; miR, microRNA; vec, vector; ERBB2, Erb-B2 Receptor Tyrosine Kinase 2; PIK3CA, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α.