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. 2017 Feb 7;114(8):E1500–E1508. doi: 10.1073/pnas.1612991114

Fig. 1.

Fig. 1.

SGK3 expression is up-regulated in ERα+ breast cancer cells during development of acquired AI resistance. (A) Relative SGK3 mRNA levels in different cell lines determined by microarray. MCF7aro-1nM T, MCF7aro cells were cultured in hormone-depleted medium and treated with 1 nM T for 48 h; TAM-R, tamoxifen-resistant MCF7aro cells, generated by long-term culture of MCF7aro cells in hormone-depleted medium added with T plus tamoxifen (>6 mo); LTEDaro, long-term estrogen-deprived MCF7aro cells, which were generated by long-term culture of MCF7aro cells in hormone-depleted medium (>6 mo), and estrogen was not required for proliferation of the resulting cells. (B) Western blotting analysis of MCF7aro cells cultured in different conditions and LET-R cells. HD, cultured in hormone-depleted medium for 48 h; T only, cultured in hormone-depleted medium and treated with 1 nM T for 48 h; regular, cultured in the normal growth medium [MEM medium with 10% (vol/vol) FBS]. LET-R cells were cultured in hormone-depleted medium and treated with 1 nM T plus 200 nM letrozole. (C) Western blotting analysis of MCF7aro cells, AI-resistant cells, and LTEDaro cells. All the cells were cultured in their normal growth media, as described in Materials and Methods. (D) Western blotting analysis of levels of SGK3 and ERα in EXE-R and LET-R cells after being treated with 100 nM ICI 182,780, 5 μM enzalutamide, or their combination for 48 h.