Li Laboratory

1. Roles of cell death factors such as caspases and necroptotic factors in cancer therapy. 

We are interested in understanding how cell death factors such as apoptotic caspases and necroptotic factors regulate host immune system response to cancer cell after cytotoxic cancer therapy such radiation therapy or chemotherapy. We aimed to uncover novel insights that can drive the development of innovative immunotherapeutic strategies.

2. Caspase-mediated cell plasticity contributes to the resistance of cancer cells to targeted therapy.

One of the cornerstones of targeted therapy in melanoma is the use of BRAF inhibitors, such as vemurafenib and dabrafenib. While these inhibitors have demonstrated significant efficacy, the development of resistance remains a critical issue. In our lab, our research shows that melanoma cells lacking Caspases are less prone to developing resistance to vemurafenib treatment. One of the mechanisms involves Caspases mediating cell plasticity, driving the reprogramming of these cells to a phenotypic state that no longer depends on the drug-targeted pathway. Our goal is to investigate how Caspases mediate cell plasticity and confer resistance to vemurafenib treatment, as well as to explore strategies to overcome this resistance.

3. Identification of novel cell signaling pathways and mechanisms that are involved in regulating tumor response to radiotherapy and ICB.

Our group recently discovered that inhibition of ATM, a key DNA double strand break repair factor, leads to enhanced type I interferon response by promoting mtDNA leakage and cGAS/STING. we hope to gain significant new insights into the roles of ATM and related factors in regulating cellular innate immunity and the tumor immune microenvironment. These new insights are likely to lead to new approaches that may significant enhance ICB and radiotherapy.