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PI3K/Akt抑制通过p35-CDK5调节促进AR活性和前列腺癌细胞增殖

Wei-Hsiang Kao1, Kun-Yuan Chiu2, Stella Chin-Shaw Tsai3

  • 1Department of Life Sciences, National Chung Hsing University, Taichung 40227, Taiwan; Translational Cell Therapy Center, China Medical University Hospital, Taichung 40447, Taiwan.

Biochimica et biophysica acta. Molecular basis of disease
|November 13, 2024
PubMed
概括

在前列腺癌 (PCa) 中,抑制PI3K/Akt激活p35-CDK5,从而增强雄激素受体 (AR) 稳定性并促进细胞存活,揭示了抵抗机制.

关键词:
这就是为什么AR AR AR AR.细胞活力 细胞活力在PI3K/Akt.前列腺癌是什么意思 前列腺癌是什么意思在p35-CDK5中使用.

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