Fig. 10

SEMA3F significantly inhibited cell proliferation, cell migration and enhanced docetaxel chemosensitivity in prostate cancer. A Endogenous SEMA3F mRNA levels in different human PCa cell lines. Data are presented as means ± SD, two-tailed unpaired t-test. B RBM15 protein was determined in PCa samples and paired adjacent normal tissues. Data are presented as means ± SD, two-tailed unpaired t-test. C Kaplan–Meier disease free survival (DFS) curves were performed from GEPIA portal. D SEMA3F protein levels are markedly decreased in human PCa cell lines compared to RWPE-1 cells. E Transwell migration assays showed the inhibition of cell migration viabilities in SEMA3F overexpression DU-145 and PC-3 cells. F Overexpression of SEMA3F significantly inhibited the cell proliferation in DU-145 and PC-3 cells, Data are presented as means ± SD, two-tailed unpaired t-test. G Pulldown followed by western blot indicated in vitro binding of m⁶A-modified RNA: DNA hybrid probe (using SEMA3F promoter sequence ) with YTHDF2 in control and IGF2BPs overexpression PC-3 cells. H Differently transfected PC-3 cells were treated with docetaxel. Cell viability was normalized to that of the corresponding cells treated with dimethylsulphoxide (DMSO). (Upper): Representative clone formation assay. (Lower): Quantification of clone formation assay. Data are represented as means ± SD. of n = 3 replicates. (I). Effect of SEMA3F overexpression on Hippo pathway in DU-145 and PC-3 cells by western blot assay. J Effect of SEMA3F overexpression and LATS1 inhibitor(TDI-011536) on Hippo pathway in DU-145 and PC-3 cells by western blot assay. K Dose–response curves of differently transfected PC-3 cells treated with docetaxel, LATS1 inhibitor(TDI-011536) and SEMA3F overexpression. Cell viability was normalized to that of the corresponding cells treated with dimethylsulphoxide (DMSO). Data are represented as means ± SD. of n = 3 replicates.  * p -value < 0.05, ** p -value < 0.01, *** p -value < 0.001, **** p -value < 0.0001