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. 2020 Mar 4;10(9):4201–4216. doi: 10.7150/thno.35589

Figure 2.

Figure 2

ERRα enhances in vitro growth resistance to androgen-deprivation and antiandrogen in prostate cancer cells. (A-D) ERRα-overexpression analysis. (A) Immunoblot validation of LNCaP-ERRα transduced clones. (B-D) In vitro growth responses of LNCaP-ERRα cells under androgen-deprivation culture condition (CS-FBS) and Enzalutamide treatment assayed by MTT. (B) Both LNCaP-pBABE and LNCaP-ERRα transduced cells grew at comparable rates in culture with normal FBS until Day-7. (C and D) However, when being cultured with CS-FBS or Enzalutamide, LNCaP-ERRα cells grew at normal rates, in sharp contrast to LNCaP-pBABE cells that did not grow. (E-H) ERRα-knockdown analysis. (E) Immunoblot validation of shERRα-transduced clones. (F-H) In vitro growth responses of LNCaP-shERRα cells toward cultures with CS-FBS and Enzalutamide as assayed by MTT. The LNCaP-shERRα cells grew at slower rate than the LNCaP-shScramble cells and did not grow in culture conditions with CS-FBS and Enzalutamide. (I-J) XCT790 treatment of VCaP cells. (I) Immunoblot analysis showed that XCT790 treatment could significantly reduce or abolish the protein level of ERRα in VCaP cells. (J-L) XCT790 treatment could significantly suppress the in vitro growth of VCaP cells cultured with CS-FBS or Enzalutamide. *, P < 0.05; **, P < 0.01 versus vector control LNCaP-pBABE, LNCaP-shScramble cells or vehicle treatment.