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首页> 外文学位 >Effect of androgen and natural compounds on proliferation of androgen-independent LNCaP human prostate cancer cells and prostate cancer progression.
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Effect of androgen and natural compounds on proliferation of androgen-independent LNCaP human prostate cancer cells and prostate cancer progression.

机译：雄激素和天然化合物对雄激素非依赖性LNCaP人前列腺癌细胞增殖和前列腺癌进展的影响。

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摘要

Both in vitro and in vivo, the proliferation of the androgen-independent human prostate cancer LNCaP 104-R1 and 104-R2 cells, derived from androgen-dependent 104-S cells after long-term androgen deprivation, is androgen-independent but suppressed by physiological concentration of androgen. These cells adapt to androgenic suppression, and revert to either androgen-simulated (R1Ad) or androgen-insensitive (R2Ad) state. Androgen receptor (AR) and prostate specific antigen (PSA) protein and mRNA expression level increases during progression from androgen-dependency to androgen-independency, but decreases during the adaptation to androgenic suppression. Over-expression AR allows both androgen-dependent and androgen-independent LNCaP cells be suppressed by androgen. Androgen down-regulates c-myc and skp2, and accumulates cell cycle inhibitor p27Kip1 that causes cell cycle G1 arrest but does not induce apoptosis in androgen-independent LNCaP cells. Besides, under androgen-depleted conditions, liver X receptor (LXR)-signaling is active and proliferation of androgen-dependent cells is inhibited, and the surviving androgen-independent cells escape from LXR-signaling by down-regulating LXR-related genes. (-)-epigallocatechin-3-gallate (EGCG) and caffeic acid phenethyl ester (CAPE) both have antiproliferative effect on LNCaP cells and may serve as alternative therapy for prostate cancer. Based on our results, androgen administration can be beneficial for the treatment of androgen-independent prostate cancer.
机译：在体外和体内，长期剥夺雄激素后，源自雄激素依赖性104-S细胞的非雄激素依赖性人前列腺癌LNCaP 104-R1和104-R2细胞的增殖均与雄激素无关，但可通过抑制雄激素的生理浓度。这些细胞适应于雄激素抑制，并恢复为雄激素模拟（R1Ad）或雄激素不敏感（R2Ad）状态。雄激素受体（AR）和前列腺特异性抗原（PSA）蛋白和mRNA表达水平在从雄激素依赖性到雄激素依赖性的过程中增加，但在适应雄激素抑制过程中降低。过量表达的AR允许雄激素抑制雄激素依赖性和非雄激素依赖性LNCaP细胞。雄激素下调c-myc和skp2，并积累细胞周期抑制剂p27Kip1，导致细胞周期G1停滞，但不诱导雄激素非依赖性LNCaP细胞凋亡。此外，在雄激素耗尽的条件下，肝X受体（LXR）信号活跃，雄激素依赖性细胞的增殖受到抑制，并且存活的雄激素非依赖性细胞通过下调LXR相关基因而逃脱LXR信号。 （-）-epigallocatechin-3-gallate（EGCG）和咖啡酸苯乙酯（CAPE）均对LNCaP细胞具有抗增殖作用，并可作为前列腺癌的替代疗法。根据我们的研究结果，雄激素给药可有益于非雄激素依赖性前列腺癌的治疗。

著录项

  • 作者

    Chuu, Chih-pin.;

  • 作者单位

    The University of Chicago.;

  • 授予单位 The University of Chicago.;
  • 学科 Health Sciences Oncology.; Biology Cell.; Biology Molecular.
  • 学位 Ph.D.
  • 年度 2005
  • 页码 149 p.
  • 总页数 149
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 肿瘤学;细胞生物学;分子遗传学;
  • 关键词

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