Date of Project


Document Type

Honors Thesis

School Name

College of Arts and Sciences



Major Advisor

Dr. Mary Huff

Second Advisor

Dr. Steven Wilt


Cadmium, a carcinogenic heavy metal, is an environmental contaminant found in air, water, and soil. It also exhibits endocrine disruptive properties by mimicking the proliferative effects of the hormone estrogen and is classified as a metalloestrogen. At low concentration levels in some cancer cells, cadmium induces cell proliferation and phosphorylation of ERK1/2, a key protein in the estrogen signaling pathway. While the signaling pathways for cadmium- induced phosphorylation of ERK1/2 have been discovered in breast and lung cancer cells, it has not yet been fully determined in ovarian cancer cells. The fairly recent discovery of a transmembrane receptor found in estrogen responsive tissues, G protein-coupled estrogen receptor (GPER), presents a possible pathway for studying cadmium’s effects in ovarian cancer cells. To determine the role of GPER in cadmium-induced phosphorylation of ERK1/2, two human ovarian adenocarcinoma cell lines, OVCAR3 and SKOV3, were treated for 30 minutes with 10 µM G15, a GPER inhibitor, followed by treatment with 100 nM CdCl2 for 10 minutes. Immunoblot analysis was performed to measure cadmium-induced phosphorylation of ERK1/2. The results indicate that in both cell lines, G-15 decreased cadmium-induced phosphorylation of ERK1/2 suggesting that GPER may be play an important role in cadmium's proliferative effect in ovarian adenocarcinomas.