CPT1A, or carnitine palmitoyltransferase 1A, is a crucial enzyme involved in the mitochondrial fatty acid oxidation (FAO) pathway, which is essential for energy homeostasis during fasting or prolonged exercise. It is responsible for the rate-limiting step of converting acyl-coenzyme as into acyl-carnitines, facilitating their transport into the mitochondria for oxidation. The regulation of CPT1A is complex and involves various genetic, epigenetic, physiological, and nutritional factors. In the context of cancer, CPT1A plays a significant role in tumor progression and metabolism. It has been found to be upregulated in various cancers, including lung cancer, and its increased expression is associated with poor prognosis. Targeting CPT1A has been proposed as a potential therapeutic strategy in cancer treatment. Inhibiting CPT1A can induce ferroptosis in cancer cells, including LCSCs, and enhance the efficacy of immune checkpoint therapy in lung cancer. Moreover, the combination of CPT1A inhibition with immunotherapy has shown synergistic effects in preclinical models, offering a new approach to overcome resistance to immunotherapy in lung cancer. Furthermore, CPT1A has been implicated in the metabolic reprogramming of cancer cells, promoting cell proliferation via nucleoside metabolism in nasopharyngeal carcinoma. It also plays a role in conferring cancer cell resistance to immune-mediated cytolytic killing.
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