Stem cells are a true double-edged sword when it comes to cancer. We need our tissue-specific stem cells to repair and replace tissue, but some of them develop into cancer causing cells. Now a CIRM-fundeed team at the University of California, Los Angeles has discovered a molecular switch that seems to keep stem cells, at least those in hair follicles, in a non-cancerous mode.
The finding has immediate implications for the most common form of skin cancer, because hair follicle stem cells initiate those cancers. But it could also apply to many other forms of stem cells and cancer.
Tissue-specific stem cells toggle between dormant and active states. Some researchers have suggested that these stem cells do not give rise to cancer in the dormant state, but they have not known what suppresses the cancer potential.
Working with mice, the team prodded hair follicle stem cells with genes known to initiate cancer, but when the cells were dormant, the cancer genes could not perform their dirty work. Once the cells starting growing, the cancer genes succeeded in starting cancer growth. They found a key gene that was active in the dormant cells and not in the growing cells. That was a gene well known to be involved in regulating the cross-talk within cells, called Pten.
The research was published online yesterday by Nature Cell Biology and a press release from UCLA quoted the first author, Andrew White, on the role of the gene:
“Stem cell quiescence is a novel form of tumor suppression in hair follicle stem cells, and Pten must be present for the suppression to work.”
He went on to suggest that better understanding of how this works could lead to cancer prevention strategies.
CIRM funding: Andrew White (TG2-01169)