Fig 2: Effect of BAY-117082 on Ki-67 expression in CAL27-xenograft model. Immunohistochemistry assay revealed that (A) control group was characterized by marked Ki-67 expression, and (B,C) treatment with BAY-117082 at doses of 2.5 and 5 mg/kg significantly reduced its expression. Data are representative of at least three independent experiments. Sections were observed and photographed at 20× and 40× magnification. (D) ## p < 0.01 vs. CTR.

Fig 3: miR-340 suppresses ovarian tumor growth in vivo.Subcutaneous xenografts of A2780 cells infected with miR-340-overexpressing lentivirus (Lv-miR-340) or control lentivirus (Lv-miR-NC) (n = 5). a Images of the tumors at autopsy from nude mice are presented. b Tumor volumes were measured at the indicated time points. c Average weight of xenografted tumors was measured. d, e Immunohistochemical (IHC) staining of Ki67 (d) and caspase-3 (e) in xenografted tumors from Lv-miR-340-A2780 cells or control cells. Magnification ×400; scale bar, 50 µm. Data are shown as means ± SD. *P < 0.05, ***P < 0.001 by two-way ANOVA or Student’s t-tests

Fig 4: MiR-873-5p exerted its role in infiltrative GC cells via targeting HNRNPK. (A–J) XGC-1 cells were transfected with miR-NC, miR-873-5p, miR-873-5p+pcDNA-NC, or miR-873-5p+pcDNA-HNRNPK. (A–E) The proliferation, migration, and invasion capacities of XGC-1 cells were analyzed by MTT, plate clone, wound-healing, or transwell assays. (F) Western blotting revealed protein levels of ki-67, E-cadherin, N-cadherin, and Vimentin in XGC-1 cells. (G and H) The ECAR and OCR of XGC-1 cells were assessed with an XF96 extracellular flux analyzer. (I and J) Glycolysis assay was performed to measure glucose uptake and lactate production in XGC-1 cells. *P < 0.05.

Fig 5: PRDM4 inhibited cell proliferation by blocking the cell cycle transition from G0/G1 to S phase.A Cell viability was determined in the PRDM4-overexpressing or PRDM4-silenced HeLa and SiHa cells by MTT assays. B Cell proliferation assays were performed in the PRDM4-overexpressing or PRDM4-silenced HeLa and SiHa cells. C, D The expression levels of PRDM4 and Ki67 in the tumor tissues are shown. E, F Cell cycle distribution was analyzed by FACS in the PRDM4-overexpressing or PRDM4-silenced cells. *p < 0.05 and **p < 0.01.