Kepeng Wang

Chronic inflammation increases cancer risk and accelerates the progression of many malignancies, including those of the lung, stomach, liver and colon. Pro-inflammatory cytokines and tumor-infiltrating myeloid and immune cells play critical roles in all stages of cancer development. Immune infiltrates are evident in most, if not all solid tumors, including those that exhibit no pre-cancer inflammation. It is now clear that the process of tumorigenesis leads to changes in tumor cells and their microenvironment. Such changes shape the quality and magnitude of immune responses to tumors, resulting in the activation of tumor-promoting inflammation and suppression of anti-tumor immunity. The nature of tumor-immune interaction is therefore under intensive study in hope to understand how cancers arise and evolve, and how we can develop novel diagnostic and therapeutic tools for the benefit of human cancer patients. Research in my lab focuses on the role of inflammation in colorectal cancer development and therapeutic intervention. Among them, IL-17 has been shown to play important roles in immunity against invading pathogens and in chronic inflammation of autoimmune diseases. IL-17 signaling also drives the development of colorectal, breast, pancreatic, and prostate cancers. Our and other people’s previous studies have shown that IL-17 signals to both tumor cells and their environment. Direct engagement of IL-17 promotes tumor cell proliferation and survival, whereas IL-17 signaling on stromal and immune cells seems to regulate tumor-associated inflammation and anti-tumor immunity. Our current study aims to address the relationship between IL-17 mediated inflammation and anti-tumor immunity, and uncover the underlying mechanism by which IL-17 regulates the activity of adaptive and innate immunity in colorectal cancer. We are also interrogating the involvement of inflammasome signaling in colorectal cancer. Our research shows a novel role of Gasdermin D in colon cancer development. Gasdermin D is an effector protein that mediates inflammasome-induced cell death, and its activation in colorectal tumors may have profound impact on the fate of tumor cells and the nature of tumor microenvironment. By studying the role of inflammation in cancer, we hope to provide additional insight on the interaction between tumor cells and their environment, and develop more effective anti-cancer therapies for the benefit of human health.

Computation-aided design of rod-shaped nanoparticles for tumoral targeting. Journal of controlled release : official journal of the Controlled Release Society 2025 Aug; 387: 114169 CARG-2020 targets IL-12, IL-17, and PD-L1 pathways to effectively treat melanoma and breast cancer. Scientific reports 2025 Aug; 15(1): 29649 Nanoscopy reveals integrin clustering reliant on kindlin-3 but not talin-1. Cell communication and signaling : CCS 2025 Jan; 23(1): 12 UBXN3B is crucial for B lymphopoiesis. EBioMedicine 2024 Jul; 106: 105248 Gut microbiota-mediated activation of GSDMD ignites colorectal tumorigenesis. Cancer gene therapy 2024 Jul; 31(7): 1007-1017 Cancer immunotherapy with enveloped self-amplifying mRNA CARG-2020 that modulates IL-12, IL-17 and PD-L1 pathways to prevent tumor recurrence.