ECE2022 Poster Presentations Environmental Endocrinology (11 abstracts)
The endocrine disruptor cadmium affects both ERα+ and ERα- breast cancer cell lines
Viviana Maria Bimonte 1 , Claudia Sabato 2 , Sofia Trocchianesi 3 , Zein Mersini Besharat 2 , Agnese Po 3 , giuseppina catanzaro 2 , Italia Falcone 4 , Alessandra Fabi 5 , Roberto Bei 6 , Michele Milella 7 , Alessandra Vacca 2 , Elisabetta Ferretti 2 & Silvia Migliaccio 1
1Foro Italico University Rome, Dept of Movement, Human & Health Sciences, Rome, Italy; 2Sapienza University Rome, Dept of Experimental Medicine, Rome, Italy; 3Sapienza University Rome, Dept of Molecular Medicine, Rome, Italy; 4IRCCS-Regina Elena National Cancer Institute Rome, Medical Oncology 1, Rome, Italy; 5Fondazione Policlinico Universitario A. Gemelli Rome, Precision Medicine in Breast Cancer Unit, Rome, Italy; 6Tor Vergata University Rome, Dept of Clinical Sciences and Translational Medicine, Rome, Italy; 7University of Verona, Section of Oncology, Verona, Italy
The highly toxic heavy metal Cadmium (Cd) is widely spread in the environment and could exert estrogen-like activity in tissues including breast. Previous studies demonstrated that Cd binds to estrogen receptor α positive (ERα+) breast cancer (BC) cells. In this new study, we evaluated effects of Cd on both ERα+ and ERα negative (ERα-) BC models with the aim to further characterize the mechanisms involved in Cd-related BC carcinogenesis. Specifically, the effect of Cd exposure was evaluated on BC cell lines MCF7 (ERα+, PR+, HER-), T47D (ERα+, PR+, HER+), and MDA-MB-231(ERα-, PR-, HER-). First of all, the effects of Cd on cell proliferation and death were evaluated. Cells treated with increasing concentrations (0.5-10 μM) of Cd showed a significant decrease in cell viability from the dosage of 5 μM after 24h in MCF7, after 48h in MDA-MB-231 and after 72h in T47D cells. The levels of steroid receptors expressed by the cells before and after Cd were also evaluated. In detail, ERα, estrogen receptor α (ERα), androgen receptor (AR), and progesterone receptor (PR) were evaluated after Cd exposure. ERα decreased in ERα+ cells while ERα expression increased in all cells. PR levels were reduced or not modulated in all cells. AR levels were increased in both ERα+ and ERα- cell models. We evaluated the ratio of AR/ERα and AR/ERα and we found that Cd induced a significant increase in the two ratios in both ERα+ and ERα- cell models. Furthermore, activation of cellular signaling pathways were evaluated. Cd induced activation of p38 MAPK in all cell lines, activation of PhAKTser473 in T47D and activation of ERK1/2 in MDA-MB-231 cells. Finally, Cd exposure induced a significant increase in the pro-inflammatory cytokines IL-6 and IL-8. In conclusion, our study demonstrates that Cd has a role in regulating cell viability, steroid receptors phenotype, cellular signaling pathways and pro-inflammatory cytokines in both ERα+ and ERα- cell models.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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