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. 2023 Jul 7;14:1188926. doi: 10.3389/fphar.2023.1188926

FIGURE 1.

FIGURE 1

Schematic of mechanisms behind anti-cancer properties of statins. Statins remove serum low-density lipoprotein cholesterol (LDL-C) by upregulating LDL receptor (LDLR) expression in liver and peripheral tissues, and downregulates cholesterol biosynthesis by suppressing mevalonate pathway via inhibition of HMG-CoA reductase (HMGCR). Reduction of cholesterol disrupts the function of lipid rafts and suppresses cancer cell proliferation. Inhibition of the mevalonate pathway by statins also reduces prenylation of proteins like Ras and RhoA GTPases, and subsequently alter multiple pathways to modulate autophagy, promote apoptosis, and suppress angiogenesis, inflammation, metastasis, etc. Statins can also modulate tumor microenvironment via promoting the activity of natural killer (NK) cells, and M2-to-M1 switch, etc. TAM, tumor-associated macrophages; IPP, isopentenyl pyrophosphate; GPP, geranylgeranyl pyrophosphate; FPP, farnesyl pyrophosphate; GGPP, geranylgeranyl pyrophosphate.