Investigating the Role of ERBB2 in Mouse Colon Tumors
Abstract
Colorectal cancer (CRC) is the second leading cause of cancer-related deaths in the United States and with the incidence of early-onset CRC on the rise, the CRC burden is rapidly shifting towards a younger population of individuals. Previous research has found that only 15% of CRC patients respond to epidermal growth factor receptor (EGFR) targeted therapies with the majority of CRCs initiating and growing faster through an EGFR-independent mechanism. This is especially the case when the cancer cells are resistant to tyrosine kinase inhibitors. ERBB2 is an understudied transmembrane growth factor receptor that is commonly upregulated in human CRC, and its precise mechanism in CRC remains largely unexplored. In our study, we obtained Gene Set Enrichment Analysis (GSEA) data to identify if there is enrichment or differential expression in a set of genes between wild type littermate control and ERBB2-deficient mice. Results have shown differential gene expression between the experimental and control mouse colon epithelial tissue, specifically enrichment in epithelial-mesenchymal transition (EMT) signaling characterized by a loss of epithelial cell markers and gain of mesenchymal markers. Subsequently, quantitative polymerase chain reaction (qPCR) results were used to validate the level of expression of EMT markers that are active in the epithelial colon tissue wild type littermate control and ERBB2-deficient mice. Determination of the mechanism of action of continued ERBB2-deficient tumor growth is an integral part to identifying potential therapeutic targets to optimize human CRC patient outcomes.
Citation
Si, Meghan Le (2023). Investigating the Role of ERBB2 in Mouse Colon Tumors. Undergraduate Research Scholars Program. Available electronically from https : / /hdl .handle .net /1969 .1 /199662.