London, May 27 (ANI): A new research by scientists from the University of Chicago and Northwestern University Feinberg School of Medicine has suggested a promising new strategy for cancer therapy.
Every cell contains machinery for self-destruction, used to induce death when damaged or sick.
But according to the new study, a receptor thought to mediate cell suicide in normal cells may actually be responsible for the unrestrained growth of cancerous tumours.
Blocking the activity of this 'death receptor' can stop and even reverse the growth of tumours in human tissue culture and mice, the researchesr have found.
Cell self-destruction, known as apoptosis, helps the body eliminate unwanted cells.
Under normal circumstances, when the death receptor called CD95 is activated by specific proteins, the process of apoptosis is triggered.
This cell suicide is an important process for immune function and to prevent the formation of uncontrolled, cancerous cell growth.
Scientists have long speculated that the loss of 'death receptors' may be an early step in the formation of tumours.
However, many cancers continue to express high levels of CD95, even as the cells rapidly grow and proliferate.
"These data raised the intriguing possibility that CD95 could actually promote the growth of tumours," said lead author Marcus Peter of Northwestern University.
The team studied the role of CD95 in tumours using several human cancer cell lines, liver cancer mouse models, and models of ovarian cancer.
Selectively deleting or reducing CD95 in these tumours dramatically slowed cell growth and, in some cases, actually killed the cells.
When researchers reduced the activator for CD95 in the cancer cell lines, the effect was even more dramatic. The tumours stopped growing; some of them even died.
Downstream targets of CD95 essential for cell growth, such as JNK, c-Fos and Egr1, also decreased their activity when the 'death receptor' was blocked.
Furthermore, treating cancer cells with JNK inhibitors caused cells to stop growing, the researchers discovered.
Further research will probe how and when the cells decide to switch the function of CD95 from 'death' to 'growth.' he study has been reported in the May 27, 2010, issue of the journal Nature. (ANI)