Our long term goal is to reveal the mechanisms by which the deregulated actin cytoskeleton promotes cancer metastasis and to develop anti-metastasis agents targeting the deregulated actin cytoskeleton in metastatic cancer cells. One critical characteristic of metastatic cancer cells is enhanced migration and invasion, which are responsible for the infiltration of metastatic cells into lymphatic and blood vessels, as well as the extravasation of cancer cells into secondary organs. The driving forces of cell migration and invasion are conferred by the actin cytoskeleton and focal adhesions that anchor actin filaments to the extracellular matrix. The researches in our lab currently focus on two interrelated projects. The first project is about fascin, an actin bundling protein. Fascin expression is very low in normal epithelia, but highly elevated in all forms of carcinoma. More importantly, high fascin levels independently predict poor clinical outcome in cancer patients. We are currently exploring the mechanism that regulates fascin expression and activity in metastatic cells. The second project is about store-operated calcium channels. We discovered that store-operared calcium channels are required for actin cytoskeleton remodeling during cancer metastasis and we are currently looking into signaling pathways downstream of calcium signaling.
The Yang lab long-term goal is to reveal the mechanisms by which the deregulated actin cytoskeleton promotes cancer metastasis and to develop anti-metastasis agents targeting the deregulated actin cytoskeleton in metastatic cancer cells. The researches in our lab currently focus on two interrelated projects. The first project is about exploring the mechanism by which fascin expression and activity in metastatic cells are regulated. The second project is about store-operated calcium channels. We discovered that store-operated calcium channels are required for actin cytoskeleton remodeling during cancer metastasis and we are currently looking into signaling pathways downstream of calcium signaling.