Fig 1: Overexpression of miR-133b inhibits proliferation and invasion in 786-O cells. (A) Transfection efficiency of miR-133 was determined using reverse transcription-quantitative PCR. (B) Cell proliferation was detected using an MTT assay following miR-133b overexpression. (C) Wound healing assay was used to investigate cell migration following miR-133b overexpression, scale bar, 200 µm. (D) Matrigel assay was used to investigate the number of invasive cells following miR-133b overexpression, scale bar, 50 µm. (E) Western blotting was used to analyze the expression levels of PCNA, MMP-2 and MMP-9 following miR-133b overexpression. *P<0.05 vs. control; #P<0.05 vs. NC. miR, microRNA; NC, negative control; PCNA, proliferating cell nuclear antigen; MMP, matrix metalloproteinase; OD, optical density.
Fig 2: Overexpressed miR-216b Inhibits Proliferation and Induces Apoptosis through Activation of the p53 Signaling by Downregulating TPX2 in cSCC(A) miR-216b expression in A431 cells determined by qRT-PCR. (B) mRNA levels of p53, p21, TPX2, and MDM2 in A431 cells determined by qRT-PCR. (C) mRNA levels of proliferation marker PCNA and apoptosis-related factors bcl-2/bax in A431 cells determined by qRT-PCR. (D) Western blots of p53, p21, TPX2, MDM2, PCNA, and bcl-2/bax in A431 cells normalized to GAPDH. (E) Protein expressions of p53, p21, TPX2, MDM2 in A431 cells determined by western blot analysis. (F) Protein expressions of PCNA and bcl-2/bax in A431 cells determined by western blot analysis. Data were expressed as mean ± standard deviation, and data among multiple groups were compared by one-way ANOVA, followed by the Tukey’s post hoc test. *p < 0.05.
Fig 3: U0126 or rapamycin inhibits the VIP-induced proliferation of granular cells and promotes oocyte apoptosis. Ovaries were cultured with (i) 10-7 mol/L VIP, (ii) VIP + 10-8 mol/L U0126 or (iii) VIP plus 8.75 × 10-8 mol/L rapamycin for 3 days. (A and D) PCNA staining and TUNEL assay were conducted for proliferation and apoptosis observation. (B) Western blot was conducted to quantify the expression of PCNA. (C and E) The numbers of primordial follicles with positive PCNA staining and oocytes with positive TUNEL staining were counted. Scale bar: 100 µm. Values are mean ± s.d. of at least three experiments. (*P < 0.05 compared with the VIP group, & P < 0.05 compared with the VIP + U0126 group, # P < 0.05 compared with the VIP + Rapa group).
Fig 4: MiR-182-5p or miR-96-5p increased HCC cell proliferation and cisplatin resistance by antagonizing RND3. (A–C): Cell viability, proliferation and apoptosis of HCC cells after indicated modifications and treatment in vitro. (D): Protein expression level of PCNA, caspase-3 and active caspase-3 in HCC treated in (A). (E–H): Cell apoptosis and caspase-3, -8 or -9 activities in HCC cells after indicated modifications and treatment in addition to cisplatin treatment in vitro. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001.
Fig 5: VIP promotes the proliferation of granular cells and inhibits the apoptosis of oocytes. Four-day-old ovaries were cultured with 10-7 mol/L VIP or VIP + VIP6–28 (5 × 10-6 mol/L) for 3 days. (A and D) PCNA staining and TUNEL assay were conducted in the three groups mentioned above for proliferation and apoptosis observation. (B) Western blot was conducted to quantify the expression of PCNA. (C and E) The percentage of primordial follicles or oocytes with PCNA-positive or TUNEL-positive section. Scale bar: 100 µm. Values are mean ± s.d. of at least three experiments. (*P < 0.05 compared with the VIP-treated group, & P < 0.05 compared with the VIP + VIP6–28-treated group).
Supplier Page from Abcam for Anti-PCNA antibody