Date Approved

2026

Degree Type

Open Access Senior Honors Thesis

Department or School

Chemistry

First Advisor

Hedeel Guy Evans, Ph.D.

Second Advisor

Harriet Lindsay, Ph.D.

Third Advisor

Ann R. Eisenberg, Ph.D.

Abstract

E-cadherin is a protein that normally helps cells adhere to each other. Sometimes, part of this protein is cleaved off and released outside the cell as soluble E-cadherin (sE-cad). When this happens, there is less E-cadherin left on the cell surface. Enzymes called matrix metalloproteases, especially MMP9, are responsible for this cleavage. In this study, we investigated E-cadherin in two non-small cell lung cancer cell lines, A549 and H1299. We found that treating these cells with brain-derived neurotrophic factor (BDNF), nicotine, or epinephrine increased the amount of MMP9 released into the surrounding media. When the cells were treated with propranolol, a drug that blocks β-adrenergic receptors, MMP9 levels decreased. In A549 cells, higher MMP9 levels were linked to higher levels of sE-cad in the media. When MMP9 was reduced in these cells, the amount of sE-cad also went down. Previous work from our lab showed that nicotine and BDNF increased cell survival, while propranolol reduced it. To understand the function of sE-cad, we removed it from the media of A549 cells. Without sE-cad, important growth and survival signals in the cells were reduced, tumor-suppressor activity increased, cell survival decreased, and cell death increased. These effects happened whether or not the cells were treated with BDNF, nicotine, or epinephrine. However, the same removal of sE-cad did not affect H1299 cells. Overall, these results suggest that soluble E-cadherin helps promote cancer cell survival and signaling in A549 lung cancer cells, but not in H1299 cells.

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