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3,3'-二吲哚甲烷对雄激素受体的下调作用有助于抑制激素敏感的LNCaP和不敏感的C4-2B前列腺癌细胞的增殖并诱导其凋亡。

Down-regulation of androgen receptor by 3,3'-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in both hormone-sensitive LNCaP and insensitive C4-2B prostate cancer cells.

作者信息

Bhuiyan Mohammad M R, Li Yiwei, Banerjee Sanjeev, Ahmed Fakhara, Wang Zhiwei, Ali Shadan, Sarkar Fazlul H

机构信息

Departments of Pathology and Internal Medicine, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.

出版信息

Cancer Res. 2006 Oct 15;66(20):10064-72. doi: 10.1158/0008-5472.CAN-06-2011.

Abstract

Despite the initial efficacy of androgen deprivation therapy, most patients with advanced prostate cancer eventually progress to hormone-refractory prostate cancer, for which there is no curative therapy. Previous studies from our laboratory and others have shown the antiproliferative and proapoptotic effects of 3,3'-diindolylmethane (DIM) in prostate cancer cells. However, the molecular mechanism of action of DIM has not been investigated in androgen receptor (AR)-positive hormone-responsive and -nonresponsive prostate cancer cells. Therefore, we investigated the effects of B-DIM, a formulated DIM with greater bioavailability, on AR, Akt, and nuclear factor kappaB (NF-kappaB) signaling in hormone-sensitive LNCaP (AR+) and hormone-insensitive C4-2B (AR+) prostate cancer cells. We found that B-DIM significantly inhibited cell proliferation and induced apoptosis in both cell lines. By Akt gene transfection, reverse transcription-PCR, Western blot analysis, and electrophoretic mobility shift assay, we found a potential crosstalk between Akt, NF-kappaB, and AR. Importantly, B-DIM significantly inhibited Akt activation, NF-kappaB DNA binding activity, AR phosphorylation, and the expressions of AR and prostate-specific antigen, suggesting that B-DIM could interrupt the crosstalk. Confocal studies revealed that B-DIM inhibited AR nuclear translocation, leading to the down-regulation of AR target genes. Moreover, B-DIM significantly inhibited C4-2B cell growth in a severe combined immunodeficiency-human model of experimental prostate cancer bone metastasis. These results suggest that B-DIM-induced cell proliferation inhibition and apoptosis induction are partly mediated through the down-regulation of AR, Akt, and NF-kappaB signaling. These observations provide a rationale for devising novel therapeutic approaches for the treatment of hormone-sensitive, but more importantly, hormone-refractory prostate cancer by using B-DIM alone or in combination with other therapeutics.

摘要

尽管雄激素剥夺疗法最初有效,但大多数晚期前列腺癌患者最终会进展为激素难治性前列腺癌,对此尚无治愈性疗法。我们实验室和其他机构之前的研究表明,3,3'-二吲哚甲烷(DIM)对前列腺癌细胞具有抗增殖和促凋亡作用。然而,DIM的分子作用机制尚未在雄激素受体(AR)阳性的激素反应性和非反应性前列腺癌细胞中进行研究。因此,我们研究了具有更高生物利用度的配方DIM(B-DIM)对激素敏感的LNCaP(AR+)和激素不敏感的C4-2B(AR+)前列腺癌细胞中AR、Akt和核因子κB(NF-κB)信号传导的影响。我们发现B-DIM在两种细胞系中均显著抑制细胞增殖并诱导凋亡。通过Akt基因转染、逆转录-聚合酶链反应、蛋白质免疫印迹分析和电泳迁移率变动分析,我们发现Akt、NF-κB和AR之间存在潜在的相互作用。重要的是,B-DIM显著抑制Akt激活、NF-κB DNA结合活性、AR磷酸化以及AR和前列腺特异性抗原的表达,表明B-DIM可能会中断这种相互作用。共聚焦研究显示,B-DIM抑制AR核转位,导致AR靶基因下调。此外,在严重联合免疫缺陷-人实验性前列腺癌骨转移模型中,B-DIM显著抑制C4-2B细胞生长。这些结果表明,B-DIM诱导的细胞增殖抑制和凋亡诱导部分是通过下调AR、Akt和NF-κB信号传导介导的。这些观察结果为设计新的治疗方法提供了理论依据,即单独使用B-DIM或与其他疗法联合使用来治疗激素敏感性但更重要的是激素难治性前列腺癌。

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