Collateral resistance to taxanes in enzalutamide‐resistant prostate cancer through aberrant androgen receptor and its variants

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  • Masaki Shiota
    Department of Urology Graduate School of Medical Sciences Kyushu University Fukuoka Japan
  • Takashi Dejima
    Department of Urology Graduate School of Medical Sciences Kyushu University Fukuoka Japan
  • Yoshiaki Yamamoto
    Department of Urology Graduate School of Medicine Yamaguchi University Ube Japan
  • Ario Takeuchi
    Department of Urology Graduate School of Medical Sciences Kyushu University Fukuoka Japan
  • Kenjiro Imada
    Department of Urology Graduate School of Medical Sciences Kyushu University Fukuoka Japan
  • Eiji Kashiwagi
    Department of Urology Graduate School of Medical Sciences Kyushu University Fukuoka Japan
  • Junichi Inokuchi
    Department of Urology Graduate School of Medical Sciences Kyushu University Fukuoka Japan
  • Katsunori Tatsugami
    Department of Urology Graduate School of Medical Sciences Kyushu University Fukuoka Japan
  • Shunichi Kajioka
    Department of Urology Graduate School of Medical Sciences Kyushu University Fukuoka Japan
  • Takeshi Uchiumi
    Department of Clinical Chemistry and Laboratory Medicine Graduate School of Medical Sciences Kyushu University Fukuoka Japan
  • Masatoshi Eto
    Department of Urology Graduate School of Medical Sciences Kyushu University Fukuoka Japan

書誌事項

公開日
2018-08-28
資源種別
journal article
権利情報
  • http://creativecommons.org/licenses/by-nc/4.0/
DOI
  • 10.1111/cas.13751
公開者
Wiley

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説明

<jats:p>Currently, the optimal sequential use of androgen receptor (<jats:styled-content style="fixed-case">AR</jats:styled-content>) axis‐targeted agents and taxane chemotherapies remains undetermined. We aimed to elucidate the resistance status between taxanes and enzalutamide, and the functional role of the <jats:styled-content style="fixed-case">AR</jats:styled-content> axis. Enzalutamide‐resistant 22Rv1 cells showed collateral resistance to taxanes, including docetaxel and cabazitaxel. However, taxane‐resistant cells showed no collateral resistance to enzalutamide; taxane‐resistant cells expressed comparable protein levels of full‐length <jats:styled-content style="fixed-case">AR</jats:styled-content> and <jats:styled-content style="fixed-case">AR</jats:styled-content> variants. Knockdown of both full‐length <jats:styled-content style="fixed-case">AR</jats:styled-content> and <jats:styled-content style="fixed-case">AR</jats:styled-content> variants rendered cells sensitive to taxanes, whereas knockdown of <jats:styled-content style="fixed-case">AR</jats:styled-content> variants sensitized cells to enzalutamide, but not to taxanes. In contrast, overexpression of full‐length <jats:styled-content style="fixed-case">AR</jats:styled-content> rendered cells resistant to taxanes. Consistently, the prostate‐specific antigen response and progression‐free survival in docetaxel chemotherapy were worse in cases with prior use of <jats:styled-content style="fixed-case">ARAT</jats:styled-content> agents compared with cases without. Collateral resistance to taxanes was evident after obtaining enzalutamide resistance, and aberrant <jats:styled-content style="fixed-case">AR</jats:styled-content> signaling might be involved in taxane resistance.</jats:p>

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