Submission Date

7-20-2017

Document Type

Paper

Department

Biochemistry & Molecular Biology

Faculty Mentor

Rebecca Roberts

Student Contributor

Jake Lachowicz

Comments

Presented during the 19th Annual Summer Fellows Symposium, July 21, 2017 at Ursinus College.

Project Description

Cancer results from genetic mutations that lead to a harmful uncontrollable cell division and differentiation. Once the cancer cells amass to a large amount, angiogenesis can turn this group of cells into a malignant tumor. The formation of new blood vessels, angiogenesis, provides a pathway for cancer cells to enter the bloodstream and metastasize to other tissues and organs in the body. Metastasis is also dependent on cathepsins, a class of lysosomal proteases secreted from cancer cells. Endocrine disrupting compounds (EDCs) are chemicals that mimic hormones and thus, disturb the endocrine system. The EDCs that are structurally similar to estrogen, such as bisphenol A (BPA), are of importance because of the key role that estrogen (17β-estradiol) plays in the growth of certain breast carcinomas. BPA, a plasticizer found primarily in polycarbonate plastics and epoxy resin linings, is able to leach from plastic products and enter the body. BPA-free products have now become widespread because of research showing the harmful effects of BPA as an EDC, such as its ability to increase the proliferation of breast cancer cells; however, there are many bisphenol analogs that are estrogenic monomers that have been used to replace BPA, such as bisphenol S (BPS) and bisphenol F (BPF). The overall purpose of this project is to determine the effects of estrogen, BPA, and bisphenol analogs on human MCF-7 breast cancer cells by examining how they affect cathepsin levels and metastasis. By understanding these interactions, we may be able to better inform the medical community about the role of bisphenols, to which we are all exposed, in the progression of breast cancer