Fig. 1

ALKBH5 overexpression promotes EOC cell proliferation and resistance to cisplatin in vitro and in vivo. (a) ALKBH5 mRNA expression is up-regulated in cisplatin-resistant EOC cells (upper); ALKBH5 mRNA expression is up-regulated in platinum-resistan EOC samples (down). (b) Results of the western-blot assays shows ALKBH5 was up-regulated both in cisplatin-resistant EOC cells (upper) and platinum-resistant EOC samples (down). (c) Expression of ALKBH5 protein in platinum-resistant (left) and platinum-sensitive (right) EOC tissues by IHC assay. (d) The transfection efficiency of oe-ALKBH5 lentivirus in A2780 and HO8910. (e and f) CCK8 and EdU proliferation assays confirm that ALKBH5 overexpression promotes cell proliferation in EOC cells. (g) The chemosensitivity assay shows that the IC50 of cisplatin is higher in EOC cells with ALKBH5 overexpression. (h) The IF assay shows that γH2AX expression is reduced in EOC cells with ALKBH5 overexpression after cisplatin treatment (5 μM, 6 h). (i) The cell cycle assays show that ALKBH5 overexpression can attenuate blocking in the G2/M phase induced by cisplatin (5 μM, 48 h). (j) The apoptosis assay shows that ALKBH5 overexpression can decrease the percentage of cell apoptosis induced by cisplatin (5 μM, 48 h). (k) The animal study shows that ALKBH5 overexpression promotes tumor growth and chemoresistance to cisplatin in vivo