Research Projects

Colorectal cancer (CRC) is a prevalent cancer with a high prevalence and poor 5-year survival rate if not diagnosed early. Dysregulation of key intracellular signaling pathways, including Wnt/-catenin, Ras, and p53 signaling, is common in CRCs. p53 protein mutations, present in about 60% of CRCs, affect patient prognosis and alter tumor biology and the tumor microenvironment. Tumor development and proliferation are fueled by p53 mutations that are either gain- or loss-of-function (LOF/GOF). Amyloid p53 can upregulate anti-apoptotic genes and downregulate pro-apoptotic genes, as well as upregulate EMT markers like vimentin and N-cadherin. Macrophages play a significant role in the response to stress, injury, infection, and inflammation. M1 macrophages are triggered by proinflammatory genes, while M2 macrophages express anti-inflammatory and tissue repair marker genes. Although p53 suppresses M2 macrophage polarization, the function of oncogenic amyloid p53 in macrophage polarization or the tumor microenvironment remains unclear.