Targeting lipid metabolism: novel insights and therapeutic advances in pancreatic cancer treatment

Table 3 The dual function of cholesterol and fatty acids in PC progression

Fatty acid or cholesterol	Tumorigenic or anti- tumorigenic function	Mechanism of action	References
Fatty acid	Anti-tumorigenic	The inhibition of fatty acid synthesis causes ferroptosis resistance	[157]
Fatty acid	Tumorigenic	Increase in fatty acid β‑oxidation and elevation in lipid droplets in pancreatic cancer, causing metastasis	[59]
Fatty acid	Tumorigenic	An increase in fatty acid synthesis reduces apoptosis	[158]
Heptadecanoic Acid, an Odd-Chain Fatty Acid	Anti-tumorigenic	Apoptosis induction Increase in gemcitabine sensitivity	[63]
Fatty acid	Anti-tumorigenic	Fatty acid suppression results in autophagy Cytoprotective autophagy subsequently increases the survival rate of cancer cells and promotes their proliferation during hypoxia	[159,160,161]
Omega-3 fatty acid	Antitumorigenic	High omega-3 fatty acid causes mitigation of cancer progression	[162]
Fatty acid	Tumorigenic	Fatty acids impair the anti-cancer function of cholesterol flux suppression	[163]
Cholesterol 25-hydroxylase	Anti-tumorigenic	Upregulation of MHC-I and increase in CD8 + T cell infiltration to exert anti-cancer immune responses	[164]
LDL cholesterol	Tumorigenic	LDL cholesterol stimulates the STAT3 axis to boost tumor cell growth	[105]
HDL cholesterol	Anti-tumorigenic	HDL cholesterol promotes cholesterol elimination to suppress the growth of tumor cells	[165]

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