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3-Ketoacyl-CoA thiolase, peroxisomal (ACAA1) is an enzyme encoded by the human *ACAA1* gene. It localizes to peroxisomes and plays a critical role in the beta-oxidation pathway, facilitating the breakdown of fatty acids into acetyl-CoA. Clinical deficiency leads to a Zellweger-like syndrome (pseudo-Zellweger). Recent research indicates ACAA1 acts as a prognostic biomarker and relates to immune cell infiltration in cancer, particularly non-small cell lung cancer, with evidence showing that oncogenic KRAS downregulates ACAA1 expression via the MAPK pathway. Its physiological and pathological roles are mostly metabolic, with increasing relevance in oncology and immunometabolism[1][2][5][6].
Inhibition (or activation) of the MAPK pathway can regulate ACAA1 expression, especially in the context of oncogenic KRAS mutations[2]
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