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. 2014 Dec 22;9(3):1287–1292. doi: 10.3892/ol.2014.2819

Figure 1.

Figure 1

Induced ABCG2 expression in HMEC-1 endothelial cells. (A) qPCR (primer, Hs01053790_m1) of ABCG2 mRNA levels in treated or non-treated HMEC-1, HMECd1, HMECd2, HMECd1r and HMECd2r cells cultured without Dox for three weeks. Sunitinib, fumitremorgin C and diethylstilbestrol were used to treat the cells. The results were obtained from three independent experiments. *P<0.05, vs. non-treated cells. (B) qPCR (primer, Hs01067802_m1) of P-gp mRNA levels in treated or non-treated HMEC-1, HMECd1, HMECd2 and HMECd2r cells. Sunitinib, fumitremorgin C, and diethylstilbestrol were used to treat the cells. The results were obtained from three independent experiments. *P<0.05 and **P<0.01, vs. non-treated cells. (C) Western blot analysis of ABCG2 levels in HMEC-1, HMECd2 and HMECd2r cells. The data for the ratio were obtained from three repeated blots. *P<0.05, vs. the control and Hd2r cells. C, HMEC-1; Hd1, HMECd1; Hd2, HMECd2; Hd1r, HMECd1r; Hd2r, HMECd2r; Su, sunitinib; F, fumitremorgin C; D, diethylstilbestrol; ABCG2, breast cancer resistance protein.