Premium
Evidence and Inhibitor Studies of Involvement of Src and EGFR in Estrogen Receptor Induced ERK1/2 Activation in Ovarian Cancer Cell Proliferation Stimulated by Cadmium Chloride.
Author(s) -
Steinke Kira,
Huff Mary
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.03609
Subject(s) - cadmium , cadmium chloride , estrogen receptor , cell growth , chemistry , cancer research , ovarian cancer , cell culture , microbiology and biotechnology , cancer , biology , medicine , biochemistry , breast cancer , genetics , organic chemistry
Cadmium Chloride, Cadmium, a naturally occurring heavy metal, is a toxic industrial and environmental pollutant commonly found in both ground and industrial waste water. Studies have shown that cadmium is also a metalloestrogen that can bind to the human estrogen receptor (ER), stimulate DNA synthesis, and increases cellular proliferation in ovarian cancer cell lines. Furthermore, it has been shown that cadmium stimulates ERK1/2 activity in an ER‐dependent manner. To determine if cadmium stimulates proliferation in ovarian cancer cell lines, OVCAR3 and SKOV3 cells were treated with varying concentrations cadmium chloride, and growth was measured by a cell proliferation assay. The results support that cadmium induces cellular proliferation at environmentally relevant concentrations (0.001–1.0 uM) within 24 hours of treatment. It was also observed that treatment with 1 nM of cadmium for 5 minutes activates ERK1/2 phosphorylation. We are now in the process of performing inhibitor studies to determine if Src and EGFR are also involved in ER dependent cadmium‐stimulated cellular proliferation in ovarian cancer cells. Support or Funding Information Bellarmine University, Student Government Association