Document Type

Poster (Access Controlled)

Publication Date

Summer 2021

Abstract

Cancerous cells arise due to genetic changes in regions of DNA that regulate cell growth, death, and/or motility causing over proliferation and formation of tumors. These cells maintain homeostasis while bypassing cell growth markers. One mechanism involved in cellular homeostasis is the 26S Proteasome which is involved in protein degradation. Some cancer treatments involve inhibition of the 26S proteasome to disrupt its function in cancer cells thus leading to cell death. Continued treatment of cancer using 26S proteasome inhibition often leads to development of resistance in cancer cells resulting in the loss of drug effectiveness. To begin to understand the mechanisms behind the cellular response to these disruptions to homeostasis, I have looked at how protein abundance levels change in Saccharomyces cerevisiae (yeast) cells containing mutations in the 26S Proteasome both with and without DNA damaging agents. By using the coding language R to analyze comparative protein abundance I can gain an insight to how cells react to DNA damage with a malfunctioning proteasome. This can provide potential targets for proteasome inhibitor resistant cancer.

Notes

Faculty Sponsor: Sarah Justice

Department: Biology

As this research is intended for eventual publication, access to this file is restricted to individuals with taylor.edu email addresses.

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