GPCR and RTK Targeting by Anti-Depressant Drug for Sarcoma in Children

Release Date: 12-Nov-2020

Cancer, among all the diseases is one of the most complex disease to treat. Therefore, number of researchers across the globe are now inclined towards conducting research that could lead to the development of efficient cancer therapies even in case of children. A group of researchers have developed some of the anti-depressants that are observed to halt the growth of cancer cells in the children suffering from sarcoma. Although the study is only conducted in mice model organisms and not in the humans but the sort of clinical outcomes received from the clinical research study is delivering tons of hopes for causing a decline in the cancer mortality rate in children.

The clinical research study included study of G protein-coupled receptors (GPCRs) and the receptor tyrosine kinases (RTKs) as these two are targeted most of the times in case of allergies, asthma, depression, anxiety and hypertension. The growth factor that is estimated to be playing an important role in case of children sarcoma is insulin-like growth factor receptor (IGF1R). Researchers involved in this respective study have shown that IGF1R shares a signalling modelling with GPCRs. This novel strategy identified by the researchers is estimated to be opening hundreds of avenues to target cancer cells in case of sarcoma. 

The researchers used the drug Paroxetine which is an anti-depressant drug that leads to the impairment of serotonin reuptake receptor that is part of the GPCR-family in mouse models. Researchers found that the drug was able to cause a decline in the number of IGF1R receptors and thereby caused a decline in the growth of tumor. The whole targeting of GPCR in case of treating sarcoma in children using an anti-depressant drug is considered as a novel paradigm for the entire cancer therapeutics sector. Now, the researchers are inclined towards developing more strategies that could involve selecting more cross-target multiple receptor tyrosine kinases and improve the clinical world.