[Prostate cancer and apoptosis].
[Prostate cancer and apoptosis].
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DOI：
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发表时间：
2011
影响因子：
0.2
通讯作者：
A. Mayora;F. Arvelo
中科院分区：
文献类型：
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作者：
A. Mayora;F. Arvelo
前列腺癌是由雄激素受体(AR)介导的雄激素依赖性生长。雄激素途径阻断是晚期前列腺癌的标准治疗方法。尽管前列腺癌最初是敏感的，但通常对激素治疗是无效的。这种抗性可能是由于AR基因扩增、AR突变和共激活蛋白表达增加所致。同样，生长因子和细胞因子可以诱导AR的磷酸化，而不依赖于配体的固定。此外，还有其他AR不依赖的途径，如神经内分泌表型的获得。在这篇综述中，我们研究了前列腺癌进展的分子机制，以及前列腺癌细胞逃避细胞凋亡的方式。
Prostate cancer presents an androgen-dependent growth mediated by the androgen receptor (AR). Androgen pathway blockage is the standard therapy for the treatment of prostate cancer at an advanced stage. In spite of an initial sensitivity, prostate cancer usually becomes refractory to hormone treatment. This resistance can be due to the amplification of the AR gene, AR mutations and the increase in co-activator protein expression. Likewise, growth factors and cytokines can induce AR phosphorylation, independently of ligand fixation. Moreover, there are other AR-independent pathways, such as the acquisition of the neuroendocrine phenotype. In this review, we examine the molecular mechanisms that are involved in the progression of prostate cancer, as well as the ways its cells evade apoptosis.