Research published in the journal Nature Structural & Molecular Biology, from scientists at the Salk Institute for Biological Studies in La Jolla, California, USA, reveals a mechanism for activating the alternative lengthening of telomeres (ALT) pathway. Cosmetic researchers in recent years have been interested in telomere-related research as they look for new approaches to stifle the effects of aging in skin.
As described by a related report in The Scientist, cancer cell immortality is dependent upon telomeres. Every time a normal cell divides, its telomeres shorten and eventually the cell’s telomeres are too short to divide. However, most cancer cells can divide indefinitely because they upregulate telomerase to lengthen telomeres—and 5% to 15% of cancers use the ALT pathway to avoid apoptosis.
Authors Roderick J. O'Sullivan, Nausica Arnoult, Daniel H. Lackner, Liana Oganesian, Candy Haggblom, Armelle Corpet, Genevieve Almouzni and Jan Karlseder found that co-depletion of the histone chaperones ASF1a and ASF1b in human cells induced all hallmarks of ALT in both primary and cancer cells. Within the study parameters, the induction of ALT led to a simultaneous suppression of telomerase.
According to The Scientist, Karlseder has future plans to knock down ASF1 in more cell lines and, eventually, in animals in order to unravel ALT pathway and successfully target telomere length or telomerase in cancer therapy. He believes his team's work can serve as a tool to initiate the development of inhibitors for the pathway, and to understand this pathway in more detail. These findings align nicely with the cosmetics industry's latest technologies targeting cell communication and genomic transcription factors for skin benefits.