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. 2014 Jan 21;7(4):1102–1108. doi: 10.3892/ol.2014.1816

Figure 2.

Figure 2

Twist2 confers resistance to cisplatin in ovarian cancer cells. (A) Validating the efficiency of pcDNA3.1(+)/Twist2 in OV2008 cells by quantitative polymerase chain reaction (qPCR). PcDNA3.1(+)/Twist2 significantly increased Twist2 at mRNA levels. (B) Validating the efficiency of si-Twist2 in C13K cells by qPCR. si-Twist2 significantly ablated endogenous Twist2 at the mRNA level. *P<0.05. (C) Validating the efficiency of pcDNA3.1(+)/Twist2 in OV2008 cells by western blotting. PcDNA3.1(+)/Twist2 significantly upregulated Twist2 at the protein level. (D) The efficiency of si-Twist2 in C13K cells was validated by western blotting. si-Twist2 significantly ablated endogenous Twist2 at the protein level. (E) IC50 level of OV2008/Twist2 induced by cisplatin was markedly higher than those of the OV2008 and OV2008/Vector cells. (F) IC50 level of C13K/si-Twist2 induced by cisplatin was markedly lower than those of C13K and C13K/si-NC cells.