Glutamine (Gln) is a non-essential amino acid that is involved in the development and progression of several malignancies, including prostate cancer (PCa). While Gln is non-essential for non-malignant prostate epithelial cells, PCa cells become highly dependent on an exogenous source of Gln. The Gln metabolism in PCa is tightly controlled by well-described oncogenes such as MYC, AR, and mTOR. These oncogenes contribute to therapy resistance and progression to the aggressive castration-resistant PCa. Inhibition of Gln catabolism impedes PCa growth, survival, and tumor-initiating potential while sensitizing the cells to radiotherapy. Therefore, given its significant role in tumor growth, targeting Gln metabolism is a promising approach for developing new therapeutic strategies. Ongoing clinical trials evaluate the safety and efficacy of Gln catabolism inhibitors in combination with conventional and targeted therapies in patients with various solid tumors, including PCa. Further understanding of how PCa cells metabolically interact with their microenvironment will facilitate the clinical translation of Gln inhibitors and help improve therapeutic outcomes. This review focuses on the role of Gln in PCa progression and therapy resistance and provides insights into current clinical trials.
谷氨酰胺（Gln）是一种非必需氨基酸，参与包括前列腺癌（PCa）在内的多种恶性肿瘤的发生与发展。虽然Gln对非恶性前列腺上皮细胞并非必需，但PCa细胞却高度依赖外源性Gln的供应。PCa中的Gln代谢受到MYC、AR和mTOR等明确致癌基因的严格调控，这些基因不仅导致治疗抵抗，还促进疾病进展为侵袭性去势抵抗性前列腺癌。抑制Gln分解代谢可阻碍PCa的生长、存活及肿瘤起始潜能，同时增强细胞对放射治疗的敏感性。因此，鉴于Gln在肿瘤生长中的重要作用，靶向Gln代谢成为开发新型治疗策略的潜在途径。目前正在进行的临床试验评估了Gln分解代谢抑制剂联合常规疗法及靶向疗法在前列腺癌等多种实体瘤患者中的安全性与有效性。进一步理解PCa细胞如何与微环境发生代谢交互作用，将有助于推动Gln抑制剂的临床转化并改善治疗效果。本综述聚焦于Gln在前列腺癌进展与治疗抵抗中的作用，并对当前临床试验进展进行探讨。
肿瘤(癌症)患者之家