Protein ‘makes cancer cells self-destruct’

A protein has been discovered which causes cancer cells to self-destruct.

US researchers have discovered it destroys up to 70% of cancer cells.

It regulates the production of a key enzyme involved in the generation of blood vessels which feed cancer cells’ growth.

The enzyme is Cox-2, which is already known to play a role in causing arthritis.

In cancer cells, it is thought to disrupt the strict timetable involved in cell production, causing proteins to be made too early or too late.

The normal cycle of cell replication and division is tightly controlled. A copy of DNA called RNA is made and that is translated into proteins - which have to be made at exactly the right time for the process to create healthy cells.

Messenger RNA (mRNA) controls the timings in cell production.

Cell survival

Researchers from Washington University School of Medicine in St Louis looked at how a protein CUGBP2 interacted with the mRNA for Cox-2 in eight types of human cancer cells.

In all eight, levels of CUGBP2 were very low, suggesting the development of cancer “turns down” the gene responsible for its production, meaning levels of the protein falls and the cancer can flourish.

But when the protein was attached to the mRNA for the Cox-2 enzyme, cancer cells could no longer make Cox-2, and they died, suggesting it plays a key role in tumour cell survival or death.

Professor Brian Dieckgraefe, co-author of the research, said: “CUGBP2 may be one type of master switch used by the cell to control other key proteins.

“Proteins like Cox-2 need to be tightly regulated to avoid uncontrolled growth. That may be why CUGBP2 levels were significantly lower in every single tumour we studied.”

Professor Shrikant Anant, who also worked on the study, said: “When CUGBP2 is introduced, there are a number of molecular derangements that take place in the cancer cell that make it susceptible to death.

“In the future, it may be possible to use this protein as a means of killing tumour cells without harming normal cells because normal cells already produce significant amounts of the protein.”

‘A step forward’

More research is underway to see if the effect seen in cancer cells is also seen in tumours. Human testing may be possible in a few years, the researchers said.

The believe CUGBP2 may help existing therapies work better.

Professor Dieckgraefe said: “Most therapeutic tools we currently use for cancer act by triggering cells to self-destruct.

“So it’s entirely possible that this might become a synergistic addition to existing therapies. By augmenting existing chemotherapy with CUGBP2, we might be able to make traditional therapies more effective.”

Dr Elaine Vickers, information officer for Cancer Research UK, said: “There has been much interest recently in the molecule Cox-2 because it is found in high levels in some cancers.

“A number of clinical trials are ongoing in the UK investigating the effectiveness of drugs that block Cox-2 in bowel cancer.

“This discovery is a step forward in our understanding of how Cox-2 is controlled.

“However, it will be many years before we know whether targeting CUGBP2 could be important in the treatment of cancer.”

The research is published in the journal Molecular Cell.

Provided by ArmMed Media
Revision date: June 14, 2011
Last revised: by Andrew G. Epstein, M.D.