Table 1.
The main fatty acid-driven mechanisms and biological effects in cancer onset, growth and metastasis.
| Entry | Implicated Mechanism | Biological Effects | Lit |
|---|---|---|---|
| 1 | Desaturation from 16:0 to 6c-16:1 (sapienic acid) | Support of membrane biosynthesis during proliferation | [29,30] |
| 2 | mTORC2 regulation of lipid metabolism | Glycolysis and lipogenesis activation | [31,32] |
| 3 | Acetyl CoA synthetase 2 promotion of acetate utilization | Maintaining cancer cell growth under hypoxia and metabolic stress | [33] |
| 4 | Adipokines mediation of ovarian cancer metastasis | Induction of lipolysis and β-oxidation to provide energy | [34] |
| 5 | Enhanced uptake of exogenous lipoproteins | (a) Cholesteryl ester accumulation, induced by PTEN loss and PI3K/AKT activation, to sustain cancer aggressiveness (b) Increased amount of cholesterol and overexpression of low-density lipoprotein receptor to boost proliferation (c) Sustaining proliferation and aggressive potential of breast cancer tumors |
[35] [36] [37] |
| 6 | Increase in lipid droplets in tumor cells | Increased COX-2 expression and storage in droplets, with effects on proliferation | [38] |
| 7 | Stearoyl CoA desaturase essentiality for cancer cell survival | Inhibition of FA desaturation, blocking the synthesis of lipids and impairing cell survival | [39] |