Indian researchers discover RTKs for treatment of colon and renal cancer

Researchers at the Kolkata-based Indian Institute of Science Education and Research (IISER) have identified the vascular endothelial growth factor receptor (VEGFR), which could pave the way for developing medical treatments for colon and renal cancer. The VEGFR family of receptors is a key regulator of the process of forming new blood vessels required for functions such as embryonic development, wound healing, tissue regeneration and tumour formation. Targeting VEGFR could help in the treatment of various malignant and non-malignant diseases.

Researchers have made a breakthrough discovery of a micromolecular process that involves a cell surface receptor related to an enzyme structure that is involved in the assembly of growth factors, regulating cell differentiation, proliferation, survival, metabolism and traffic, as well as preventing cancer. This enzyme, called VEGFR1, prevents itself from growing in the absence of a ligand, such as a hormone. This research could significantly pave the way towards therapeutic solutions for colon and kidney cancers using molecules that primarily stabilize the inactive state of VEGFR1.

Cell surface receptors such as receptor tyrosine kinases (RTKs) are critical for translating extracellular signals (from chemical signals such as growth factors, commonly referred to as ligands) into a regulated cellular response. Ligand binding to extracellular receptors activates intracellular coupled enzymes (tyrosine kinases). The activated enzyme, in turn, adds a phosphate group to several tyrosine molecules that act as an adaptor to assemble a signaling complex. The formation of signaling complexes regulates diverse cellular functions such as cell growth, development, and immune response. Spontaneous activation of RTKs in the absence of ligand is often associated with many human pathologies such as cancer, diabetes, and autoimmune disorders. Researchers are exploring how a cell maintains the autoinhibited state of the enzyme and why such autoinhibition occurs during the progression of human pathologies.
Source