Fig. 2 | Oncogene

Fig. 2

From: Orphan nuclear receptor TLX contributes to androgen insensitivity in castration-resistant prostate cancer via its repression of androgen receptor transcription

Fig. 2

TLX overexpression enhances both in vitro and in vivo androgen deprivation-resistant growth capacity in AR-positive prostate cancer cells. a Immunoblot validation of stable TLX infectants generated from AR-positive LNCaP, LAPC-4 and VCaP cells. b–d In vitro growth responses of LNCaP-TLX infectants to charcoal-stripped fetal bovine serum (CS-FBS) and bicalutamide treatments. e In vitro growth responses of LAPC-4-TLX infectants to bicalutamide and CS-FBS. Data are presented as mean ± SD of triplicate assays. f, g In vivo tumorigenicity assay. f In vivo growth response of LNCaP-vector infectants and LNCaP-TLX xenograft tumors to host castration. Tumors formed by LNCaP-TLX infectants continued to grow aggressively in castrated hosts, whereas tumors formed by LNCaP-pBABE infectants ceased to grow upon castration. g Upper panel: graph shows the wet weights of dissected tumors formed by LNCaP-TLX and LNCaP-vector infectants, collected at 18 weeks after s.c. inoculation into intact host SCID mice, which were castrated at 9 weeks post inoculation. Lower panel: photograph shows the dissected tumors formed by the representative inoculated infectants. LNCaP-TLX infectants formed significantly larger tumors than LNCaP-vector infectants in castrated animals. *P < 0.05 versus LNCaP-vector infectants. Data are presented as mean ± SD of quadruplicate measurements

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