Fig. 3.

TACC2 is associated with hormone-dependent prostate cancer cell proliferation by accelerating the M-phase transition. A, Silencing of TACC2 mRNA by siRNA. LNCaP cells were transfected with siControl 1 and 2 or siTACC2 1 and 2 (5 nm each). TACC2 mRNA levels were analyzed by real-time PCR. The data represent the mean ± sd, n = 2. B, siRNA-mediated knockdown of TACC2 protein. LNCaP cells were transfected with siControl 1 or siTACC2 1 and treated with R1881 (10 nm) for 48 h. Whole-cell lysates were immunoblotted with anti-TACC2 and anti-β-actin. C, TACC2 knockdown retards LNCaP cell proliferation. LNCaP cells were transfected with siControl or siTACC2 (5 nm each). The MTS assay was performed 1–3 d after transfection. The data represent the mean ± sd, n = 4. *, P < 0.05 from siControl 1. D, TACC2 knockdown suppresses androgen-dependent growth of LNCaP cells. The MTS assay was performed 1–5 d after treatment with vehicle or DHT (10 nm) (siRNA transfection was performed 48 h before ligand treatment). The data represent the mean ± sd., n = 4. *, P < 0.01 from siControl transfection with DHT treatment. E, TACC2 knockdown increases G₂/M phase cells. LNCaP cells were transfected with siControl or siTACC2 and subjected to cell cycle analysis by FACS, 96 h after transfection. Each percentage of G₂/M phase cells is described in the graph. Representative result of repeated three experiments is shown.