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. Author manuscript; available in PMC: 2018 Jul 15.
Published in final edited form as: Clin Cancer Res. 2017 Feb 14;23(14):3906–3917. doi: 10.1158/1078-0432.CCR-16-2530

Figure 5.

Figure 5

Role of MUC16 in cisplatin and gemcitabine resistance. A & B, We treated MUC16 knockdown (H292-shMUC16 seq1 and seq2) and scramble (H292-SCR) cells with various concentrations of cisplatin and gemcitabine. MTT assay results show that MUC16 knockdown (P<0.05) cells were more responsive to cisplatin (A) and gemcitabine (B). C & D, Similarly, MUC16-Cter overexpressed cells (P<0.05) were more resistant to cisplatin (C) and gemcitabine (D). E & F, Muc16 knockdown (K1418-shMuc16) mouse GEMM tumor cells (P<0.05) were more sensitive to cisplatin (E) and gemcitabine (F) than scramble cells. Mechanism of MUC16 mediated chemoresistance. G, Upon MUC16 knockdown, expression of p53 was increased as compared to scramble. H, The expression of p53 was high in tumors derived by subcutaneous injection of MUC16 knockdown cells as compared to tumors derived by injection of scramble cells. I, Similarly, MUC16-Cter overexpressed cell had a lower p53 expression. β-actin was used as loading control. *P<0.05, **P<0.01, ***P<0.001, and NS non-significant. I, Figure magnification 20X.