Understanding the role of GPCR65-dependent metabolic communication in the tumor microenvironment (01)

• Subject Area: Immunology ; Dermatology
• Term: since 2018
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 318346496

The tumor mass consists not only of a heterogeneous population of cancer cells but also a variety of resident and infiltrating host cells, secreted factors and extracellular matrix proteins, collectively known as the tumor microenvironment (TME), influencing anti-tumor immune responses. In this context, we were able to show that the high metabolic demand of cancer cells leads to acidification of the TME. Our detailed molecular analyses demonstrated this acidification is sensed by G protein-coupled receptor (GPCR)65 on macrophages, polarizing these cells towards a tumor-promoting phenotype. Hence, this project is focused on a detailed understanding of GPCR65 biology.

• DFG Programme: Collaborative Research Centres
• Subproject of: SFB 1292: Targeting convergent mechanisms of inefficient immunity in tumors and chronic infections
• Applicant Institution: Johannes Gutenberg-Universität Mainz
• Project Heads: Professor Dr. Tobias Bopp; Professor Dr. Edgar Schmitt, until 12/2021