Author ORCID Identifier

0000-0002-4616-089X

Date of Graduation

5-2025

Document Type

Thesis (MS)

Program Affiliation

Biomedical Sciences

Degree Name

Masters of Science (MS)

Advisor/Committee Chair

Don L. Gibbons, M.D., Ph.D.

Committee Member

Swathi Arur, Ph.D.

Committee Member

Lauren Byers, M.D.

Committee Member

Samuel Mok, Ph.D.

Committee Member

Kartik Venkatachalam, Ph.D.

Abstract

Lung cancer is the leading cause of cancer-related deaths in the United States, largely due to its ability to metastasize. Epithelial-to-mesenchymal transition (EMT) is a process that enhances the ability of cells to lose their cell-cell contacts, invade, and enter the blood stream which are essential during metastasis. Many transcriptional gene programs are altered during EMT such as activation of mesenchymal transcription factors, like ZEB1, and enhanced response to the TGFβ1 cytokine. In oncogenic contexts, TGFβ1 enhances the formation of processing-bodies (P-bodies) where P-body proteins are required for invasion in multiple cancerous cell lines. P-bodies are a type of ribonucleoprotein (RNP) granule that assist in post-transcriptional gene regulation by storing or degrading mRNAs. However, the role of P-bodies has not been examined in lung cancer. This led to the hypothesis that EMT induces P-body formation where P-bodies reciprocally regulate EMT and invasion in lung cancer cells. Here, the author describes novel discoveries on the strong correlation between P-body formation and various EMT mechanisms in lung cancer cells despite P-bodies being non-essential for EMT or invasion. This study provides a foundation for future research to elucidate the mechanistic function of P-bodies during EMT in cancer progression.

Keywords

Non-Small Cell Lung Cancer, Lung Adenocarcinoma, Epithelial-to-Mesenchymal Transition, Ribonucleoprotein, Processing-body, RNA Binding Protein, Transforming Growth Factor β, AU-rich element, Decapping mRNA 1a, Stress Granule

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