Document Type

Honors Thesis

Date of Award

Fall 2023

Abstract

Breast cancer is one of the most common cancers worldwide with millions of cases diagnosed each year. Despite modern treatments, over 40% of patients can expect to relapse after initial cancer eradication. Consequently, it is crucial to unravel the mechanisms by which breast cells confer their cancerous properties to develop novel treatments that improve patient survival. G1P3 is a mitochondrial localized protein found to be upregulated 50x in estrogen receptorpositive breast cancer and is correlated with overall poor patient survival. G1P3-overexpressing cells display increased amounts of interferon-stimulated genes (ISGs) and G1P3 as an ISG indicates these genes potential to promote cancerous activity. Recently, it has been found that G1P3 encourages the association of Rab5-containing endosomes (RCEs) with mitochondria. Thus, it was hypothesized that the direct interaction between G1P3 and Rab5 promotes the association of RCE-mRNA complexes with mitochondria to enhance the translation of ISGs. To determine if G1P3 and Rab5 were forming a protein complex a co-immunoprecipitation was performed. However, it was determined Rab5 and G1P3 were not directly associated to facilitate the RCE-mitochondrial interaction. Preliminary results of quantitative RT-PCR suggest that more ISG RNA is present in Co-IP samples. Overall, these results indicate other interactions are responsible for the RCE-mitochondrial interaction, though more research is needed to determine what these interactions are and what purpose the complex serves in conferring cancerous properties to breast cells.

Advisor

Venu Cheriyath

Included in

Biology Commons

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