Arginine Deprivation Induces Quiescence and Confers Vulnerability to Ferroptosis in Colorectal Cancer.

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Tác giả: Hao Chen, Junguo Chen, Shuang Guo, Hui He, Xiaosheng He, Tianze Huang, Ping Lan, Guanman Li, Yanyun Lin, Danling Liu, Kai Wang, Liang Xu, Bin Zhang, Yanhong Zhang

Ngôn ngữ: eng

Ký hiệu phân loại: 949.59012 *Greece

Thông tin xuất bản: United States : Cancer research , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 676988

Metabolic reprogramming is a hallmark of cancer. Rewiring of amino acid metabolic processes provides the basis for amino acid deprivation therapies. In this study, we found that arginine biosynthesis is limited in colorectal cancer (CRC) due to the deficiency of ornithine transcarbamylase (OTC). Accordingly, CRC cells met the demand for arginine by increasing external uptake. The addiction to environmental arginine resulted in the susceptibility of CRC to arginine deprivation, which dramatically decreased proliferation in CRC cells and promoted these cells to enter a reversible quiescence state. Arginine deprivation induced quiescence by activating the AMPK-p53-p21 pathway. RNA sequencing data indicated that CRC cells may be vulnerable to ferroptosis during arginine deprivation, and the combination of ferroptosis inducers and arginine deprivation strongly impeded tumor growth in vivo. These findings suggest that dietary modification combined with ferroptosis induction could be a potential therapeutic strategy for CRC.
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