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. Author manuscript; available in PMC: 2022 Oct 13.
Published in final edited form as: Oncogene. 2022 Apr 13;41(20):2824–2832. doi: 10.1038/s41388-022-02307-9

Figure 4. KIF20A-driven cell proliferation and tumor growth depends on AR signaling.

Figure 4.

(A) Cell proliferation of LNCaP (N = 3) and LAPC4 (N = 2) EV or KIF20A cells cultured in 5% CSS. On day 3 (denoted by the black arrow), 10 μM Enzalutamide was added to the media. (B) LNCaP KIF20A or (C) VCaP KIF20A xenografts were randomly assigned to daily treatment arms, Vehicle (LNCaP, N = 7; VCaP, N = 8) or 10 mg/kg Enzalutamide (LNCaP, N = 8; VCaP, N = 6). Prostate Specific Antigen (PSA) was measured from blood plasma at the end of treatment. (D) RTqPCR of the AR target gene (FKBP5) was analyzed from LNCaP or VCaP KIF20A tumors from mice treated with enzalutamide or vehicle. (E) Ki67 and (F) CD31 immunohistochemistry quantification and representative 10x images exported from the OlyVIA software are shown. (G) RTqPCR (N = 4) of AR target genes (FKBP5, KLK3) was performed after LNCaP EV or KIF20A cells were deprived of androgens and cultured in 5% CSS for 3 hrs. (H) Luciferase assays (N = 3) with MMTV (containing androgen or glucocorticoid response elements) or ΔGRE (lacking response elements) plasmids were conducted in LNCaP EV or KIF20A cells cultured in 5% CSS. The ratios of luciferase values (MMTV/ΔGRE) were normalized to protein concentrations. (I) AR protein in LNCaP EV or KIF20A cells was quantified (N = 4) and normalized to Actin. T tests were performed. ns = not significant * p < 0.05; ** p < 0.01. Error bars = SEM