Date Presented

Fall 12-17-2018

Document Type

Thesis

Access Type

1

Degree Name

Bachelor of Science

Department

Biomedical Science

First Advisor

Allison Jablonski

Second Advisor

Nancy Cowden

Third Advisor

Jason Crumpton

Abstract

When the cell surface molecule, Human EGF Receptor (HER2), is overexpressed, the cell can become cancerous. MDA-MB-453 is an established breast cancer cell line made cancerous by HER2 overexpression. This mutation that causes HER2 overexpression affects the cell signaling pathway of phosphoinositide 3-kinase (PI3K), Akt, MDM2, and p53. We predicted that PI3K would be inhibited with the compound, LY294002, sending signals for Akt and MDM2 to be deactivated in MDA-MB-453 cells. Deactivated MDM2 signals for p53 to be activated. P53 is a tumor suppressor protein that exists in low quantities in normal cells, but when damage occurs, p53 expression rises. Its function is to recognize mutations, regulate cell proliferation, and induce apoptosis when genetic material is mutated (Ng, Khoo, Heng et al., 2011). The effects of PI3K inhibition were determined through an XTT assay, which indicates cell density, and a Western blot, to determine the presence of activated p53. The results of the research showed that after exposure to PI3K inhibitor, LY294002, cell proliferation did decrease and acetylated p53 was present, indicating apoptosis as the cause of death.

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