Investigating the role of p53 amyloid in the tumor associated macrophage polarization and tumor microenvironment of colorectal carcinoma
Implementing Organization
AMITY University, Noida, Uttar Pradesh
Principal Investigator
Dr. Shinjinee Dasgupta
AMITY University, Noida, Uttar Pradesh
CO-Principal Investigator
Dr. Venkatesh V Kareenahalli
Indian Institute of Technology (IIT)
CO-Principal Investigator
Prof. Subhrajit Biswas
AMITY University, Noida, Uttar Pradesh
CO-Principal Investigator
Dr. Sonia Kapoor
AMITY University, Noida, Uttar Pradesh
Project Overview
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.
AMITY University, Noida, Uttar Pradesh
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