Inflammatory foci are hypoxic, and this focal hypoxia can drive the inflammatory cascade. The significance of this bidirectional crosstalk and the mechanistic role of hypoxia in inflammation is a major goal in our laboratory. Through studying the role of HIF in mouse models of inflammation, our studies demonstrate that HIF signaling is critical in regulating the epithelial inflammatory response.

Our work clearly demonstrates that regulation of epithelial elicited inflammation through modulation of HIF response plays an essential role in tissue injury. Moreover, our recent data using genetic mouse models and cell lines have shown that hypoxic signaling is a critical regulator of colon and liver cancer. Recently, in mouse models of cancer, we demonstrated that HIF2a signaling is activated rapidly and is important for tumor inflammation. HIF2a-induced pro-inflammatory response is essential for colon cancer progression.