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

Figure 3.

Figure 3

ERRα overexpression promotes in vivo castration-resistant growth capacity and enhances intratumoral androgen levels in LNCaP-ERRα-derived xenograft tumors. (A) Images show the representative castrated SCID mice bearing the xenograft tumors formed by LNCaP-ERRα and LNCaP-pBABE cells and the dissected xenograft tumors formed by the corresponding cells after 1-month growth in castrated host. (B) Growth curve shows the growth responses of LNCaP-ERRα and LNCaP-vector clones in intact host mice for initial 9 weeks followed by 4-week growth in same hosts after castration. LNCaP-ERRα clones formed larger tumors than vector clones in intact mice before castration and continued to grow aggressively in castrated hosts, as compared to tumors formed by LNCaP-pBABE clones that became atrophied after host castration. (C) Measurement of wet weights of xenograft tumors. LNCaP-ERRα clones formed tumors heavier than their vector counterpart in castrated hosts. (D) Measurement of androgens in xenograft tumors by LC-MS/MS. Significant higher levels of testosterone and DHT were detected in LNCaP-ERRα-derived tumors as compared to its vector counterpart. Data are represented as mean ± SD (n = 5) and analyzed by Students' t-test. *, P < 0.05; **, P < 0.01 versus vector control LNCaP-pBABE cells.