The Role of Lipid Metabolism in the Progression of Head and Neck Cancers

Current knowledge of fat metabolism in cancer progression has not been completely characterized. Fat depletion has been reported to be associated with poorer prognosis independent of body mass index. Inflammatory cytokines such as interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and interleukin-1 beta (IL-1β) produced by the tumor or immune cells have been linked to dysfunction of adipose tissues. On the other hand, biologically active lipid mediators, such as prostaglandins and leukotrienes have been implicated in cancer progression. The knowledge of how these proinflammatory cytokines and lipid mediators orchestrate the complex interactions between adipose tissues and cancer cells is crucial for understanding tumor progression and metastasis. Observations from our preliminary data showed that mediators released from human primary adipocytes that undergone lipolysis promoted cancer cell growth and this growth-promoting effect might through the activation of mTOR/p70S6K1 pathway. On contrary, mediators from healthy adipocytes suppressed cancer cell growth and inhibited activation of p70S6K1, STAT3, and NF-kB in cancer cells. We speculated that the tumor load initiates the inflammatory events of adipose tissues and both the released lipid mediators and the proinflammatory cytokines or adipokines contribute to tumor progression. In this study, we aimed to clarify the impacts of fat compositions on the tumor progression of head and neck patients, as well as to identify the critical lipid mediators and their interactions between adipocytes and cancer cells

Project ID:PC10408-1725
External Project ID:MOST104-2320-B182-016