Date of Project


Document Type

Honors Thesis

School Name

College of Arts and Sciences



Major Advisor

Dr. Mary Huff

Second Advisor

Dr. Amanda Krzysiak

Third Advisor

Dr. Steven Wilt


Cadmium, a heavy metal and carcinogen, is an environmental and workplace contaminate. As a known endocrine disruptor, it can mimic the proliferative effects of estrogen and is classified as a metalloestrogen. While the proliferative effect of estrogen on cancerous cell growth has been well established, the effects of cadmium have not been fully examined. To determine if cadmium stimulates growth in two human ovarian adenocarcinoma cell lines, OVCAR3 and SKOV3, cells were treated for 48 hours with varying concentrations of cadmium, 0.001 µM – 10 µM, and growth was measured using a cell proliferation assay. Both cell lines showed a peak in cellular proliferation at 0.1 µM, and cell death was induced at 10 µM. Further, cadmium was shown to activate phosphorylation of ERK1/2, a key protein involved in estrogen signaling. To determine if cadmium-induced phosphorylation of ERK1/2 uses a similar signaling pathway as estrogen, inhibitors were used to block two key proteins in the estrogen signaling pathway including the estrogen receptor (α and ß) and MEK. Following treatment with each inhibitor, cells were treated with cadmium for five minutes, and immunoblot analysis was used to measure the level of ERK1/2 phosphorylation. Preliminary results suggest the inhibition of MEK decreases ERK1/2 phosphorylation in SKOV3 and OVCAR3 cell lines. However, results demonstrate that inhibiting the estrogen receptors α and ß does not inhibit phosphorylation of ERK1/2, suggesting cadmium induces cellular changes using a different pathway than estrogen.