Repurposing of an Approved Drug for the Inhibition of Tumor Progression

 Overview

The development of metastases in vital organs is the leading cause of death in cancer patients.

Execution of the EMT (epithelial mesenchymal transition) program is the suggested mechanism by which carcinomas gain the ability to metastasize and become chemo resistant. Therefore, inhibition of this process will result in cells that will form fewer metastatic colonies and are more sensitive to anti-cancer drugs.

There are two therapeutic approaches to target the EMT program:

Developing drugs that selectively target only the mesenchymal cells.

Developing drugs that prevent the execution of the EMT program or reverse the EMT phenotypes through mesenchymal-epithelial transition (MET).

Indeed, several drugs that prevent the EMT are suggested. However, these drugs have limitations: they were developed to inhibit specific cancer-driving mutations and they target signaling pathways that are not unique to the EMT program.

Our innovation

Our drug is an endogenous compound that provides a significant advantage over the other drugs by functioning as an EMT-suppressor independent of cancer drivers. Our study demonstrates that a certain metabolite is sufficient to inhibit cancer cell migration and we found a major actor in the EMT-activation process.