Fig 2: Influential effects of AR silencing on the expression of QKI. The protein and mRNA expression levels of AR, PSA and QKI were detected by western blotting and reverse transcription-quantitative polymerase chain reaction, respectively, in (A) LNCaP and (B) C4-2 cells. ß-actin served as an internal control to ensure equal loading. The data are expressed as the mean ± standard deviation (n=3). *P<0.05 and **P<0.01. AR, androgen receptor; QKI, quaking; PSA, prostate-specific antigen; si, small interfering.

Fig 3: Dynamic changes of QKI with androgen deprivation therapy. Representative western blot images of protein expression levels of AR, PSA and QKI in (A) LNCaP and (B) C4-2 cells. (C) The mRNA expression levels of AR, PSA and QKI were determined using RT-qPCR in LNCaP and C4-2 cells. (D) The mRNA expression levels of ARv567es, AR-V7 and their target gene UBE2c in C4-2 cells upon androgen deprivation treatment determined using RT-qPCR in C4-2 cells. Data are expressed as the mean ± standard deviation (n=3). *P<0.05 and **P<0.01. AR-, cells cultured with charcoal stripped serum; AR+, cells cultured with charcoal stripped serum and dihydrotestosterone; QKI, quaking; AR, androgen receptor; PSA, prostate-specific antigen; RT-qPCR, reverse transcription-quantitative polymerase chain reaction.

Fig 4: Effects of QKI gene on cell cycle- and apoptosis-associated proteins and the AR antagonist drug Casodex in prostate cancer cells. The effects of QKI silencing on the cell cycle- and apoptosis-associated proteins in (A) LNCaP and (B) C4-2 cells. (C) The effects of QKI silencing on bicalutamide sensitivity. The data are expressed as the mean ± standard deviation (n=3). *P<0.05, **P<0.01 and ***P<0.001. QKI, quaking; si, small interfering; ctrl, control; CXD, Casodex.

Fig 5: Expression of AR and QKI in prostate cancer cell lines, clinical samples and AR binding elements in QKI promoter region. (A) Protein levels of QKI in the two prostate cancer cell lines LNCaP and C4-2 were detected by western blotting. β-actin served as an internal control to ensure equal loading. (B) mRNA expression levels of QKI in the above cell lines were quantified by reverse transcription-quantitative polymerase chain reaction, and β-actin served as an internal control to ensure equal loading. (C) The protein expression of AR and QKI in prostate cancer samples. (D) AR binding elements in the QKI promoter region were detected by a dual-luciferase reporter system. Data are expressed as the mean ± standard deviation (n=3). **P<0.01 and ***P<0.001. AR, androgen receptor; QKI, quaking; si, small interfering.