LXR ACTIVATION IMPAIRS ESTRADIOL DEPENDENT PROLIFERATION IN HUMAN BREAST CANCER CELLS THROUGH DOWNREGULATION OF GENE EXPRESSION ASSOCIATED WITH DNA REPLICATION AND CELL CYCLE PROGRESSION

OLSZANOWSKI E; OGARA MF; NACHT A. S.; RODRIGUEZ SEGUÍ S; VICENT G.P.; PECCI A.

Mar del Plata

Congreso; LXXII Reunion Anual de SAIC; 2022

SAIC

iver X Receptors (LXRs) belong to the nuclear receptors superfamilyof ligand activated transcription factors, whose endogenousagonists are the oxysterols. They play a key role in the regulation ofthe cholesterol homeostasis, induce the de novo synthesis of triacylglycerides,and counteract pro-inflammatory effects. LXRs are alsoknown to compromise cell proliferation in several cancer models.However, their role in breast cancer (BC) has not been studied indepth and reports are, in fact, contradictory. Here we examined thepotential involvement of LXRs in BC cells with special emphasis ontheir possible crosstalk with the Estrogen Receptor alpha (ERɑ). Toaddress this objective, we performed colony formation (CFA) andpropidium iodide staining assays in MCF-7 cells treated with orwithout Estradiol (E2) and the LXR agonist, GW3965. Our resultsshowed that GW3965 impared the cell proliferation capacity inducedby E2 (CFA: #colonies, Mean±SD: E2 208.7±25.7; E2+GW3965131.3±23.7, n=3, padj