The Role of Peroxisome Proliferator-Activated Receptor-b/d (PPARb/d) in Transforming Growth Factor b-Induced Epithelial-Mesenchymal Transition (EMT) of Human Lung Adenocarcinoma Cell Line

Open Access
Ali, Ayesha S
Area of Honors:
Biochemistry and Molecular Biology
Bachelor of Science
Document Type:
Thesis Supervisors:
  • Jeffrey Maurice Peters, Thesis Supervisor
  • Sarah Ellen Ades, Honors Advisor
  • Richard John Frisque, Faculty Reader
  • cancer
  • human lung adenocarcinoma
  • lung
  • ppar-b/d
  • tgf-b
Epithelial-mesenchymal transition (EMT) is necessary during certain stages of development; however, it can be detrimental when acquired by tumor cells. Epithelial mesenchymal transition can allow tumor cells to invade to surrounding tissues resulting in metastasis, and subsequent tumors can resist apoptic agents making the cancer very aggressive. Transforming Growth Factor-β (TGFβ), which induces epithelial mesenchymal transition, facilitates this transition. Peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) is a ligand-activated transcription factor that regulates proliferation and differentiation among other processes in the cell. The role of PPARβ/δ is controversial but there is some evidence that PPARβ/δ promotes terminal differentiation of epithelial tissues. This study examined the effect of ligand activation of PPARβ/δ ligand GW0742 on TGFβ-induced epithelial mesenchymal transition in human lung adenocarcinoma cell line A549. Epithelial mesenchymal transition was assessed by observing changes in the morphology of the cells and measuring the expression of proteins involved in epithelial mesenchymal transition, such as E-CADHERIN and VIMENTIN by western blot analysis. The analysis of morphology did not show the suppression of TGFβ-induced epithelial mesenchymal transition in A549 cells post- or co-treated with PPARβ/δ agonist. The results from western blot analysis were inconclusive due to inadequate amounts of protein. Therefore, the experiments conducted in this study must be repeated and additional studies with PPARβ/δ overexpressed cells treated with specific ligands should be completed.