Inhibition of Fatty Acid Amide Hydrolase Inhibits Tumor Growth in a Murine Model of Breast Cancer



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It has been shown that endocannabinoids exert a pro-apoptotic effect on cancer cell lines which typically have mutated apoptosis mechanisms. It is known that FAAH is a downstream regulator of endocannabinoid levels which degrades them into inactive fatty acids and ethanolamine. By inhibiting FAAH using the inhibitor URB 597, we can harness the body’s natural production of endocannabinoids to encourage apoptosis in cancer cells. We have shown through in vitro models that FAAH is present in breast cancer and increased apoptosis can be achieved through the addition of exogenous endocannabinoids and URB 597. Here, we develop an in vitro model of breast cancer using GFP & luciferase transduced breast cancer cells and an immune-deficient mouse model. After establishing breast cancer tumors and treating with URB 597, we are able to show that the inhibition of FAAH also results in decreased proliferation and increased apoptosis in breast cancer cells in vivo.



Breast cancer, Mouse Model, Apoptosis, Endocannabinoids, Proliferation, Fatty Acid Amide Hydrolase, FAAH, EGFR, URB 597, Matrigel, In vivo, In vitro