The emerging metabolic role and treatment target of CPT1A in CRC.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing biological mechanisms and preclinical findings without systematic review or original human data
PubMed 42597308 · doi:10.3389/fcell.2026.1881073
What was done
This narrative review summarizes published literature on the biological functions of carnitine palmitoyltransferase 1A (CPT1A) and its mechanistic role in fatty acid oxidation, metabolic reprogramming, and colorectal cancer (CRC) progression.
What was found
The abstract reports no numerical data or effect sizes. It qualitatively describes that CPT1A promotes CRC progression by regulating oncogenic signaling pathways, enhancing cancer stemness, supporting tumor proliferation and metastasis, modulating oxidative stress, altering protein modifications (histone acetylation and lysine succinylation), and shaping the tumor microenvironment.
Why it matters
The paper frames CPT1A-driven fatty acid oxidation as a key metabolic vulnerability and potential therapeutic target in colorectal cancer.
Limits
As a narrative review, it lacks a systematic search methodology, quantitative meta-analytic pooling, and risk of bias assessments. The discussed mechanisms rely predominantly on preclinical and cellular models rather than direct human clinical trial outcomes.
Cited by
- supports Carnitine palmitoyltransferase (CPT) is the rate-limiting enzyme for transporting fatty acids into the mitochondria for beta-oxidation.