Johns Hopkins logo Prior attempts to understand the mechanism of cancer proteins and find a suitable tumor suppressor in the human cancer cells have seemingly not yielded any significant results. It was discovered that instead of finding its way to the cells membranes and curbing cancer replication, the proteins would evidently loll around in the cellular broth.

Finally this maze has been understood by Meghdad Rahdar, a cell biologist in the Johns Hopkins University School of Medicine. Rahdar apparently genetically clasped at the protein’s tail, which compelled the protein to go about its activity of compressing the tumor cells.

Rahdar says, “It was curious that when we removed its tail, the protein suddenly was unhindered and moved out to the membrane and became active.” Professor and director of cell biology at Johns Hopkins, Peter Devreotes says this new approach may probably pave the path for the further development of treatments in cancer therapy. He says, “A long-term goal is to find a drug that does the equivalent of our bit of genetic engineering.”

The tail of the protein is evidently believed to consist of four amino acids, which are responsible for the functionality of this tumor suppressor, called the PTEN. On getting chemically modified, apparently these amino acids take effect in order to “glue” the PTEN’s tail back to its body, and also curb the closure of the PTEN to the membrane.

The process of genetically removing PTEN’s tail, the PTEN gets enabled to move on to the cell membrane. Here the PTEN evidently gets back to work by degrading the PIP3 molecular signal, which is responsible for cell growth.

Rahdar says that the act of genetically manipulating cancer cells may not be the safest, practical approach; however the same manipulation in PTEN can be done through drugs. This approach may prove to be a hindrance for cancer cell replication.

This research was supported by the National Institutes of Health.

These findings are published online in the Proceedings of the National Academy of Sciences.