Date Approved

2025

Degree Type

Open Access Senior Honors Thesis

Department or School

Chemistry

First Advisor

Hedeel Evans, Ph.D.

Second Advisor

Ann R. Eisenberg, Ph.D.

Abstract

We previously found that the levels of soluble amyloid precursor protein α (sAPPα) are partly regulated by acetylcholinesterase (AChE) in human non-small cell lung cancer cell lines A549 (p53 wild-type) and H1299 (p53-null). In this study, we hypothesize that sAPPα is partly regulated by leptin, a hormone classically recognized for its anorexigenic role in appetite regulation— yet recently shown to play a role in cancer cell signaling. It was observed that cells treated with leptin exhibited greater concentrations of sAPPα and lower concentrations of Aβ40/42 in the media compared to those of cells left untreated. An opposite effect was observed with cells in which leptin, or its receptor, was knocked down. It was also observed that cells treated with leptin increased ACh levels and decreased the activity of AChE and p53 in the cells. In addition, it was observed that leptin led to increased activities of PKC, ERK1/2, and PI3K in the cells. Lastly, leptin also appeared to lead to increased cell viability of the cells. The discoveries of this study emphasize the power of leptin in cancer cell metabolism, underscoring the importance of investigating it as a potential target of therapeutic agents in the future.

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