Cyclin-dependent kinase 12 deficiency reprogrammes cellular metabolism to alleviate ferroptosis potential and promote the progression of castration-resistant prostate cancer
Haozhe Zhang , Yi Zhou , Yating Feng , Wenli Hou , Yafei Chen , Zengzhen Xing , Yifan Zhang , Qiang Wei , Yu Yin , Ju Guo , Hailiang Hu
Clinical and Translational Medicine ›› 2024, Vol. 14 ›› Issue (5) : e1678
Cyclin-dependent kinase 12 deficiency reprogrammes cellular metabolism to alleviate ferroptosis potential and promote the progression of castration-resistant prostate cancer
• CDK12 deficiency promotes castration-resistant prostate cancer (CRPC) progression by reprogramming cellular metabolism. • CDK12 deficiency in CRPC leads to a more active mitochondrial electron transport chain (ETC), ensuring efficient cell energy supply. • CDK12 phosphorylates RNA Pol II to ensure the transcription of ACSL4 to regulate ferroptosis. • Mitochondrial ETC inhibitors exhibit better selectivity for CDK12-deficient CRPC cells, offering a promising new therapeutic approach for this subtype of CRPC patients.
CDK12 / CRPC / ferroptosis / metabolism
2024 The Authors. Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.
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