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

EVELYN OLSZANOWSKI; MARÍA FLORENCIA OGARA; A. SILVINA NACHT; SANTIAGO ANDRÉS RODRÍGUEZ-SEGUÍ; GUILLERMO P. VICENT; ADALI PECCI

MAR DEL PLATA - BUENOS AIRES - ARGENTINA

Congreso; Reunión Anual de Sociedades de Biociencias 2022; 2022

Sociedad Argentina de Investigación Clínica (SAIC), la Sociedad Argentina de Inmunología (SAI) y la Sociedad Argentina de Fisiología (SAFIS)

Liver X Receptors (LXRs) belong to the nuclear receptors superfamily of ligand activated transcription factors, whose endogenous agonists are the oxysterols. They play a key role in the regulation of the cholesterol homeostasis, induce the de novo synthesis of triacylglycerides, and counteract pro-inflammatory effects. LXRs are also known to compromise cell proliferation in several cancer models. However, their role in breast cancer (BC) has not been studied in depth and reports are, in fact, contradictory. Here we examined the potential involvement of LXRs in BC cells with special emphasis on their possible crosstalk with the Estrogen Receptor alpha (ERɑ). To address this objective, we performed colony formation (CFA) and propidium iodide staining assays in MCF-7 cells treated with or without Estradiol (E2) and the LXR agonist, GW3965. Our results showed that GW3965 impared the cell proliferation capacity induced by E2 (CFA: #colonies, Mean±SD: E2 208.7±25.7; E2+GW3965 131.3±23.7, n=3, padj