Abstract
Resveratrol (Resv) offers health benefits in cancer and has been reported to modulate important enzymes of lipid metabolism. Studies of its effects on lipid composition in different subtypes of breast-cancer cells are scarce. Thus, we investigated the alterations in phospholipids (PL), fatty acids (FA), and lipid metabolism enzymes in two breast-cancer cell lines after Resv treatment. MCF-7 and MDA-MB-231 cells were treated with 80 and 200 μM of Resv, respectively, for 24 hours. We analyzed PL with radiolabeled inorganic phosphate (32Pi) by thin-layer chromatography, FA by gas chromatography-mass spectrometry, and lipid metabolism enzymes (DGAT2, FAS, ρACCβ, pAMPKα, and AMPK) by Western blot. Resv treated MDA-MB-231 phospholipids showed a reduction in phosphatidylcholine (63%) and phosphatidylethanolamine (35%). We observed an increase in eicosapentaenoic acid (EPA) (73%) and docosahexaenoic acid (DHA) (65%) in MCF-7 cells after Resv treatment. Interestingly, the same treatment caused 50% and 90% increases in EPA and DHA, respectively, in MDA-MB-231 cells. In MCF-7 cells, Resv increased the expression of ρACCβ (3.3-fold) and AMPKα/ρAMPKα (1.5-fold) and in MDA-MB-231 cells it inhibited the expression of ρACCβ (111.8-fold) and AMPKα/ρAMPKα (1.2 fold). Our results show that Resv modified PL and saturated and unsaturated FA especially in MDA-MB-231 cells, and open new perspectives to the understanding of the reported anticancer effect of Resv on these cells.
Highlights
Tumors share a common phenotype of uncontrolled cell proliferation and for this they must efficiently generate energy and biomass components to expand and disseminate
The importance of lipid metabolism for the maintenance of tumor cells and the modulation of fat homeostasis by resveratrol [1, 4] are known, interestingly, this relationship has not yet been studied in these two cell lines. us, the present study aims to analyze the effect of Resv on phospholipids, fatty acids, and lipid metabolism enzymes in MCF-7 and MDA-MB-231 cells
After 8 h, we observed a reduction of PL content (518 CPM) in relation to control (1155 CPM), and this difference in biosynthesis was accentuated after 24 h of treatment (1992 CPM for treated and 5181 CPM for control cells)
Summary
Tumors share a common phenotype of uncontrolled cell proliferation and for this they must efficiently generate energy and biomass components to expand and disseminate. Cancer cells with high proliferation rates need lipids in larger quantities. Cancer preclinical models and clinical trials have revealed the crucial role of lipid classes and molecular species in supporting tumor growth and metastatic dissemination [2]. Changes in lipid metabolic pathways to perturb lipid homeostasis through the targeting of enzymes, receptors, or bioactive lipids induce tumor regression and inhibit metastatic spread [1]. We can highlight tamoxifen, an antiestrogen used in first-line endocrine therapies for estrogenpositive (ER+) breast cancer, acting to inhibit phospholipid (PL) metabolism, leading to apoptosis [3]. Plant-derived bioactive compounds such as resveratrol (Resv), may modulate lipid metabolism [4]
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