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Curcumin provides potential protection against the activation of hypoxia and prolyl 4-hydroxylase inhibitors on prostate-specific antigen expression in human prostate carcinoma cells

Authors

  • Li-Chuan Chung,

    1. Department of Bioengineering, Tatung University, Taipei, Taiwan
    2. Department of Anatomy, Chang Gung University, Tao-Yuan, Taiwan
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    • These authors contributed equally to this work.

  • Ke-Hung Tsui,

    1. Department of Urology, Chang Gung Memorial Hospital, Tao-Yuan, Taiwan
    2. Bioinformation Center, Chang Gung Memorial Hospital, Tao-Yuan, Taiwan
    3. School of Traditional Chinese Medicine, Chang Gung University, Tao-Yuan, Taiwan
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    • These authors contributed equally to this work.

  • Tsui-Hsia Feng,

    1. School of Nursing, Chang Gung University, Tao-Yuan, Taiwan
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  • Shiow-Ling Lee,

    1. Department of Bioengineering, Tatung University, Taipei, Taiwan
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  • Phei-Lang Chang,

    1. Department of Urology, Chang Gung Memorial Hospital, Tao-Yuan, Taiwan
    2. Bioinformation Center, Chang Gung Memorial Hospital, Tao-Yuan, Taiwan
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  • Horng-Heng Juang

    Corresponding author
    1. Department of Anatomy, Chang Gung University, Tao-Yuan, Taiwan
    2. Bioinformation Center, Chang Gung Memorial Hospital, Tao-Yuan, Taiwan
    • Chang Gung University, 259 Wen-Hua 1st Road, Kwei-Shan, Tao-Yuan 333, Taiwan, ROC Fax: +886-3-2118112
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Abstract

Scope: Prostate-specific antigen (PSA) is a well-known marker for diagnosing and monitoring prostate cancer. Curcumin, a yellow curry pigment, has been reported to enhance androgen receptor (AR) degradation. We examined the effects of curcumin on increasing PSA expression by hypoxia and prolyl hydroxylase inhibitors, L-mimosine and dimethyloxalylglycine (DMOG), in human prostate carcinoma LNCaP cells.

Methods and results: The 3H-thymidine incorporation assay revealed that either L-mimosine or DMOG treatments attenuated cell proliferation. Immunoblot and enzyme-linked immunosorbent assays (ELISA) indicated that both L-mimosine and DMOG have an effect similar to hypoxia, which stabilized hypoxia-inducible factor-1α (HIF-1α) and induced PSA gene expression. The results of the immunoblot and transient gene expression assays indicated that induction of the PSA expression by hypoxia is both HIF-1α- and AR-dependent. Immunoblot assays revealed that a curcumin treatment (10 μM) decreased the protein abundance of AR but did not significantly affect the protein levels of HIF-1α and vascular endothelial growth factor, which were induced by hypoxia. ELISA and transient gene expression assays indicated that curcumin blocked the activation of L-mimosine or DMOG treatment on PSA expression.

Conclusions: These results indicate that curcumin blocked the enhanced effect of PSA expression by L-mimosine and DMOG that induce hypoxia condition.

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