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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 2.

Figure 2

Stable of knockdown of MUC16 and ectopic overexpression of MUC16-Cter in lung cancer cells and its role in lung cancer cell growth and tumorigenicity. A & B, MUC16 is endogenously present in both H292 and H1975 lung cancer cells and its expression was silenced using pSUPER-Retro shRNA method with two different targets (shMUC16 seq1 and shMUC16 seq2). D & E, The growth of MUC16 knockdown cells (shMUC16 seq1 and shMUC16 seq2) was significantly (P<0.05) reduced. C, We ectopically overexpressed MUC16-Cter (F114HA) in MUC16 negative lung cancer cell A549. F, MUC16-Cter overexpressed lung cancer cells (A549-F114HA) had a higher growth rate (P<0.05) than vector-transfected (A549-CMV9) cells. G, We performed tumorigenic assay by sub-cutaneously injecting MUC16 knockdown and scramble in athymic mice. MUC16 knockdown cells (H292-shMUC16 seq1 (P=0.007) and seq2 (P=0.04) had significantly less tumorigenic capacity than scramble (H292-SCR) cells. H, MUC16 expression was low in tumors induced by MUC16 knockdown (H292-shMUC16 seq1 and seq2) cells as compared to scramble (H292-SCR) cells. β-actin was used as loading control. *P<0.05, **P<0.01 and ***P<0.001, and NS non-significant. H, Figure magnification 20X.