A promising method for promoting programmed cell death (apoptosis) developed by researchers at the Hebrew University of Jerusalem and the Weizmann Institute of Science paves the way for a possible novel therapy to target cancer cells.

Programmed cell death is an essential process in the living organism, but in many cases, cancer cells are not susceptible to this process due to mutations in genes encoding for apoptosis-related proteins.

This leads to survival of the cancer cells, which overtake normal healthy cells.

Apoptosis is a complex process mediated by networks of many proteins that interact with each other in various pathways. Of these proteins, a particularly important family is the BCL-2 protein family. Its members are the major regulators of mitochondrial apoptosis.

Mitochondria are organelles (specialised subunits within the cells) that play a critical role in cellular metabolism. 

Collaborative research between the laboratories of Prof. Assaf Friedler from the Institute of Chemistry at the Hebrew University and Prof. Atan Gross from the Department of Biological Regulation at the Weizmann Institute focused on studying in detail the interaction between two key proteins involved in apoptosis: the tBID protein, which belongs to the BCL-2 family and acts as a critical regulator of apoptosis, and the MTCH2 protein, which was recently identified in Gross’s laboratory.

Using a variety of techniques, the sites that mediate the interactions between the two proteins were identified, and the exact mechanism by which the interaction occurs was revealed. Based on this, the researchers developed peptides (short protein fragmets), derived from the interaction sites, that killed cancer cells.

The researchers concluded, therefore, that the interaction between tBID and MTCH2 is a novel target for developing anti-cancer drugs. The research, which was performed mainly by Hebrew University Ph.D student Chen Hener-Katz, was published recently in the Journal of Biological Chemistry.

Source: Hebrew University of Jerusalem