The Effects of Leptin Treatment on STAT/AKT/ERK Signaling Pathways in CRL2091 Fibroblast and HT1080 Fibrosarcoma Cells
Area of Honors:
Veterinary and Biomedical Sciences
Bachelor of Science
Sagarika Kanjilal, Thesis Supervisor Dr. Lester C Griel Jr., Honors Advisor
Leptin obesity cancer ObRb STAT Akt ERK STAT3 ERK1/2 AKT1/2/3 signaling leptin receptor fibroblast fibrosarcoma
The hormone leptin has been known to play an integral role in the development of obesity. More recent research has led to the discovery of the association between circulating leptin levels and the development and progression of carcinomas in various organ sites. It has been demonstrated that binding of leptin to its receptor on carcinoma cells leads to phosphorylation and activation of signaling proteins enhancing cellular proliferation, survival, migration, and invasion. However, the effect of leptin on normal and cancer cells of mesenchymal origin has been largely unknown. We hypothesized that leptin effects mesenchymal cells by activating signal transduction pathways and conducted experiments with a view to elucidating the effects of leptin on the phosphorylation status of STAT3, ERK1/2, and AKT1/2/3 in fibroblast (CRL2091) and fibrosarcoma (HT1080) cells. The results of the study confirm the hypothesis and start to provide mechanistic insights on the observed leptin-induced increase in proliferation, migration, and invasion of leptin treated CRL 2091 and HT1080 cells.