Abstract
Hepatocellular carcinoma (HCC) stands as a severe malignant tumor with a profound impact on overall health, often accompanied by an unfavorable prognosis. Despite some advancements in the diagnosis and treatment of this disease, improving the prognosis of HCC remains a formidable challenge. It is noteworthy that lipid metabolism plays a pivotal role in the onset, development, and progression of tumor cells. Existing research indicates the potential application of targeting lipid metabolism in the treatment of HCC. This review aims to thoroughly explore the alterations in lipid metabolism in HCC, offering a detailed account of the potential advantages associated with innovative therapeutic strategies targeting lipid metabolism. Targeting lipid metabolism holds promise for potentially enhancing the prognosis of HCC.
Abbreviations
27HC, 27-hydroxycholesterol; ABCA1, ATP-binding cassette transporter A1; ABCG1, ATP-binding cassette transporter G1; ACAT1, acetyl-CoA acetyltransferase 1; ACC, acetyl-CoA carboxylase; ACLY, ATP-citrate lyase; ACSS, acetyl-CoA synthetase; AMPK, AMP-activated protein kinase; AT, acyltransferase; CACT, carnitine-acylcarnitine translocase; CD36, fatty acid translocase; CEs, cholesteryl esters; ChREBP, carbohydrate-responsive element-binding protein; COA, coenzyme A; COMMD10, cu and copper metabolism murr1 domain 10; CPT, carnitine palmitoyltransferase; DAG, diacylglycerol; DGAT, DAG acyltransferase; EMT, epithelial-mesenchymal transition; ER, endoplasmic reticulum; FABPs, FA-binding proteins; FAO, Fatty acid oxidation; FAs, fatty acids; FASN, fatty acid synthase; FATPs, fatty acid transport proteins; FPP, farnesyl pyrophosphate; G-3-P, glycerol-3-phosphate; GPX4, glutathione peroxidase 4; HCC, Hepatocellular carcinoma; HDL, high-density lipoprotein; HIF, Hypoxia-Inducible Factor; HMG-CoA, 3-hydroxy-3-methyl glutaryl CoA; HMGCR, HMG-CoA reductase; HMGCS, HMG-CoA synthase; IHC, Immunohistochemical; IPP, isopentenyl pyrophosphate; LDL, low-density lipoprotein; LDLR, LDL receptor; LDs, Lipid droplets; LOX, lipoxygenase; LPA, lysophosphatidic acid; LXR, liver X receptor; MBOAT, membrane-bound O-acyltransferase; MUFA, monounsaturated fatty acids; MVA, mevalonate; NAFLD, nonalcoholic fatty liver disease; NASH, non-alcoholic steatohepatitis; NK, natural killer; PUFAs, polyunsaturated fatty acids; ROS, reactive oxygen species; SCD, Stearoyl-Coenzyme A Desaturase; SFAs, saturated fatty acids; SOAT, Sterol O-acyltransferase; SOCS2, suppressor of cytokine signaling 2; SQLE, squalene monooxygenase; SR-B1, scavenger receptor class B type 1; SREBPs, sterol regulatory element-binding proteins; STK25, Serine/threonine protein kinase 25; TACE, transarterial chemoembolization; TAG, triacylglycerol; TCA, tricarboxylic acid; TME, tumor microenvironment.
Disclosure
The authors report no conflicts of interest in this work.