The emerging metabolic role and treatment target of CPT1A in CRC
TL;DR
The biological functions of CPT1A are summarized, its mechanistic role in CRC progression is discussed, its emerging potential as a metabolic and therapeutic target in CRC is highlighted, and increasing evidence suggests that targeting CPT1A may be a promising therapeutic strategy for CRC.
Abstract
Fatty acid oxidation is a major metabolic pathway responsible for fatty acid breakdown and energy production. Carnitine palmitoyltransferase 1A (CPT1A), the rate-limiting enzyme in this process, catalyzes the conversion of acyl-coenzyme A into acyl-carnitine, enabling mitochondrial transport for oxidative metabolism. Emerging evidence indicates that dysregulated CPT1A contributes to metabolic disorders and cancer progression by driving metabolic reprogramming, modulating oxidative stress, and regulating protein modifications, including histone acetylation and lysine succinylation. Colorectal cancer (CRC), one of the leading causes of cancer-related mortality worldwide, has recently been linked to aberrant CPT1A activity. Studies demonstrate that CPT1A promotes CRC progression by regulating oncogenic signaling pathways, enhancing cancer stemness, supporting tumor proliferation and metastasis, and shaping the tumor microenvironment. Increasing evidence suggests that targeting CPT1A may be a promising therapeutic strategy for CRC. In this review, we summarize the biological functions of CPT1A, discuss its mechanistic role in CRC progression, and highlight its emerging potential as a metabolic and therapeutic target in CRC.