Fig. 3

CSRP2BP enhances cervical cancer cell proliferation in vitro and in vivo. A CSRP2BP protein levels in three cervical cancer cell lines (Hela, SiHa and C-33A) and ANTs (ANT1 and ANT2) were examined by Western blotting. B, C Stable overexpression and knockdown of CSRP2BP in Hela and C-33A cell lines were evaluated by Western blotting and RT‒PCR. D-E The effect of CSRP2BP overexpression or knockdown on the proliferation of Hela and C-33A cells was examined by cell growth curve and colony formation assays. In cell growth curve, the relative cell number was expressed as the fold change relative to that on Day 0. The data are presented as the mean ± SD. Statistical significance was assessed by a two-tailed Student’s t test. F EdU assays were performed to evaluate the proportion of cells in cell cycle S-phase (n = 6, scale bar 20 µm). G Cell cycle flow cytometric analysis of CSRP2BP overexpressing/knockdown Hela/C-33A cells and vector control cells. H Generation of the xenograft model in BALB/c-nude mice. Hela-CSRP2BP, Hela-shCSRP2BP and the respective control cells were inoculated into BALB/c-nude mice (n = 5/group). Representative MRI images of the tumours (top). I-K Tumour volume and weight were significantly increased in Hela-CSRP2BP cells. Compared with that in the control group, volume of tumours derived from Hela-shCSRP2BP cells was significantly smaller. Data are shown as the mean ± SD (n = 5, scale bar 1 cm). L H&E staining of representative samples derived from mouse xenografts. The trends in CSRP2BP expression and Ki-67 staining by IHC were consistent (Scale bar 50 µm). M, N CSRP2BP enchances cervical cancer proliferation and induces chemoresistant. A Flow cytometry analysis of annexin V + /PI cells after the indicated cells were treated with cisplatin (20 µg/ml, 40 µg/ml and 80 µg/ml) for 24 h. Results were expressed as percentages of apoptosis cells. All experiments were repeated at least 3 times independently with each carried out in triplicate. (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001)