My research focuses on the molecular mechanisms underlying lung cancer and lung fibrosis. For many years my work primarily focused on proteases and adhesion receptors coordinate cell invasion and extracellular matrix remodeling, especially integrin signaling. I led the first discovery of the physical and functional connections between integrins and the key cell surface protease, plasminogen activator. After moving from Harvard to UCSF, I was committed to understanding and targeting the emerging relationship between hypoxia, EMT, and tissue remodeling during fibrogenesis and cancer progression. I pioneered the in vivo investigation of the role of epithelial mesenchymal transition (EMT) in pulmonary fibrosis and uncovered mechanistic insight as to how integrins and hypoxia regulate epithelial cell plasticity. In the past few years, I have been focusing on cell-based high throughput screen of TGFbeta1 inhibitors and identified small molecules that inactivate lysyl oxidase activity and selectively block TGFbeta1 responses in tumor cells and fibroblasts. These compounds greatly attenuated pulmonary fibrosis and blocked lung cancer metastasis in mouse disease models. I have led the efforts to the dissection of MOAs of the lead compounds and I am the main contributor to the pilot clinical study of the lead compound on blocking fibrotic biomarkers in patient lungs with Idiopathic Pulmonary Fibrosis (IPF). My future goal is to bring the most promising drug candidate that specifically blocks the TGFbeta1-induced collagen program in fibroblasts to the clinical arena.