T4 INDUCES THE PROLIFERATION OF HORMONE-SENSITIVE MAMMARY TUMOR CELLS

CANO ROCIO YASMIN; FERRANDO MATIAS; ZYLA, LEILA E.; BRUNA, FLAVIA A.; SANTIANO, FLAVIA E.; CREYDT, VIRGINIA PISTONE; FONTANA, CONSTANZA LÓPEZ; CARÓN, RUBÉN W.

Mendoza

Congreso; XL Reunión Científica Anual de la Sociedad de Biología de Cuyo; 2022

Sociedad de Biologia de Cuyo

Each year, approximately 17,000 women are diagnosed with breast cancer (BCa) and 5,400 women die from this cause in Argentina.Mendoza, which has a slightly higher incidence of BCa than the national average, is considered an endemic goiter area. There is controversyabout the relationship between thyroid disorders and BCa risk, and little molecular data based on in vitro studies is available.Hypothyroidism seems to be a protective factor against BCa but long-term exposure or overdoses of thyroid replacement therapy withthyroxine (T4) may increase BCa risk. In previous studies, we observed that hypothyroidism prolonged the latency of tumor appearance,reduced tumor incidence, and retarded tumor growth in rats. In addition, we demonstrated that T4 regulated mammary carcinogenesis byinteracting with other hormone pathways. In the present study, we analyzed the biological activity of T4, alone or combined with othersteroid hormones, on the proliferation, viability, and adhesion of human BCa cell lines. MCF-7 (REα+, REβ+, PgR+, TRβ1+) and MDAMB-231 (REα-, REβ-, PgR-, TRβ1-) were treated with 10-9 M of T4; 17β estradiol (E2) and/or progesterone (P4) in DMEM/F12 with 1%of charcoalized fetal bovine serum (FBSc) or DMEM/F12 with 1% FBSc as control. We evaluated proliferation and adhesion by MTT,and viability by trypan blue. Statistical analysis was performed using ANOVA I and Bonferroni as post test (p