Open Access

Ratio of the expression levels of androgen receptor splice variant 7 to androgen receptor in castration refractory prostate cancer

  • Authors:
    • Yoshitaka Sekine
    • Hiroshi Nakayama
    • Yoshiyuki Miyazawa
    • Seiji Arai
    • Hidekazu Koike
    • Hiroshi Matsui
    • Yasuhiro Shibata
    • Kazuto Ito
    • Kazuhiro Suzuki
  • View Affiliations

  • Published online on: October 13, 2021     https://doi.org/10.3892/ol.2021.13092
  • Article Number: 831
  • Copyright: © Sekine et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

In clinical samples, the expression of androgen receptor (AR) and of AR splice variant 7 (AR‑V7) is higher in castration‑resistant prostate cancer (CRPC) compared with that in hormone‑sensitive prostate cancer (PCa). However, there are only a few reports on the ratio of the expression levels of AR‑V7 to AR (AR‑V7/AR) in prostate tissue. The present study evaluated AR‑V7/AR expression in various types of human prostate tissues and CRPC cells. Pretreatment prostate tissue samples from patients with benign prostatic hyperplasia (BPH; n=18), Gleason score 7 (n=17), and Gleason score 8‑10 (n=26) were collected at the time of prostate biopsy, and tissue samples from CRPC patients (n=10) were collected at the time of transurethral resection of the prostate. Furthermore, androgen‑independent LNCaP cells were established. The mRNA expression levels of AR and AR‑V7, cell proliferation and prostate‑specific antigen (PSA) production were evaluated by reverse transcription quantitative PCR, MTS assay and chemiluminescent enzyme immunoassay, respectively. There was a significant difference in AR‑V7/AR expression ratios between the CRPC group and the BPH and pre‑treatment PCa groups (CRPC, 7%; BPH and pre‑treatment PCa, 1%). Subsequently, we compared the AR and AR‑V7 expression levels in CRPC samples with those in the pretreatment prostate tissues from the same patients. The results demonstrated that the AR‑V7/AR ratio increased from 3 to 9% after CRPC onset. Furthermore, in vitro experiment demonstrated that AR‑V7 expression in LNCaP cells was increased after transforming into CRPC cells. The AR‑V7/AR ratio also increased from 0.05 to 0.3%. In addition, small interfering (si)‑RNA‑mediated knockdown of AR inhibited the proliferation of and PSA production from androgen‑independent LNCaP cells; however, AR‑V7 knockdown had no effect. Conversely, siRNA‑mediated knockdown of both AR and AR‑V7 inhibited the proliferation of VCAP cells. In summary, the findings from the present study demonstrated that AR‑V7 expression and AR‑V7/AR ratio were increased after the onset of CRPC, which had a limited role in CRPC cell proliferation. Further investigation is required to clarify the roles of AR other splice variants and AR‑V7 in CRPC.
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