Loss of tumor suppressive properties of lipid metabolism enzyme CPT2 in ovarian carcinoma: Comment on “CPT2 down-regulation promotes tumor growth and metastasis through inducing ROS/NFκB pathway in ovarian cancer” by Zhang et al.

Abstract Lipid metabolism is an essential process in cancer growth and progression. It is highly relevant in tumors with an adipocyte-rich microenvironment, such as ovarian carcinoma (OC). Carnitine palmitoyltransferase 2 (CPT2) is a key enzyme in fatty acid oxidation (FAO) that functions as a tumor suppressor in OC. Downregulation of CPT2 is reportedly associated with poor prognosis of OC patients. At the cellular level, low CPT2 translates into reduced NADPH level and unopposed reactive-oxygen species (ROS)/nuclear factor kappa B (NFκB) signaling which are paralleled by induction of mesenchymal mediators, invasion and metastasis. While strategies to propagate the tumor suppressive properties of CPT2 have yet to be developed, a comprehensive approach of co-assessment and co-targeting of CPT2 and its family member CPT1, or/and other key FAO players with FAO-specific inhibitors or/and less specific inhibitors (e.g. targeting NFκB, STAT3) is worth pursuing to improve understanding of the metabolic aspects of OC and develop a lipid metabolism-centered therapeutic strategy that can benefit OC patients.