Cancer cells don't die as they should

The proteins, called Pak1 and DLC1, appear to work together to promote the survival and spread of the disease.

A team from the University of Texas says targeting either one of the proteins may be enough to trigger cancer cells to self-destruct.

The research is published in the journal Cancer Cell. Cancer Research UK called it "potentially very exciting".

The results of this study are potentially very exciting. Dr Emma Croager

The researchers have found that Pak1 triggers a tiny chemical change in its partner in crime.

The modified form of DLC1 seems to sabotage the signalling mechanism within cells that triggers their suicide at the end of their natural life.

As a result breast cells continue to survive, multiply, and spread. The loss of ability to respond to cell death signals is a hallmark of cancer.

The researchers examined breast tumours from 60 patients.

They found that 54 contained elevated levels of DLC1.

In mice genetically engineered to over-produce DLC1, cells were found to move faster than normal, reproduce more quickly, and grow without normal cell-to-cell contacts.

However, more detailed analysis showed that five out of six of the human samples contained the form of DLC1 which had lost its ability to tell cells to die.

Drug target

Lead researcher Professor Rakesh Kumar said: "We might be able to develop a small molecule, a drug that could target the business end of this protein to interfere with the transformation process."

The research team engineered a form of the DLC1 protein missing the crucial site that is modified by contact with Pak1.

This form of the protein could no longer block cell death signals and could no longer form tumours.

However Professor Kumar said more research was needed to understand how over-production of DLC1 contributes to the development of breast cancer.

Dr Emma Croager, Science Information Officer at Cancer Research UK, said: "Once cancers spread to other parts of the body, they are much more difficult to treat successfully.

"Understanding how and why cancers spread is important if we are to improve the outlook for cancer patients.

"The results of this study are potentially very exciting, particularly as more than 90% of human breast tumours produce high levels of the target molecule DLC1.

"These are early findings and further research is needed to see if blocking the function of DLC1 can stop the growth and spread of breast cancer in people."