Taming Cancer telomerase

Tumor telomerases can be turned off using alternative splicing

Kirill Stasevich, Compulenta

Almost all cancer cells have one thing in common: they have too much of the enzyme telomerase. Telomerase is known to restore telomeres, the end sections of chromosomes that shorten after each division. The length of telomeres determines the life span of a cell: when the end sections are completely "eaten" by regular division, it is the turn of important genes, without which the cell cannot live. Damage to these genes, which are no longer covered by telomeres, leads to disease and cell death.

But in cancer cells with telomeres, everything is OK thanks to an increased level of telomerase. And many researchers believe that the problem of cancer can be solved if it were possible to suppress the activity of this enzyme in malignant cells. Scientists from the Southwest Medical Center of the University of Texas (USA) offer their own way of taming cancer telomerases. RNA that is synthesized on the telomerase gene can undergo alternative splicing, that is, its blocks can be mounted in different ways, and as a result, several protein variants can be obtained from the same gene.

However, most of these telomerase variants are inactive. And, more importantly, the regulatory area that determines the course of splicing is outside the coding region and has an unusual sequence. This makes it easy to interfere with the control of telomerase RNA splicing and incline it to an inactive form. How alternative splicing of telomerase RNA occurs and how it depends on an external regulatory site, scientists tell on the pages of Cell Reports (Wong et al., Regulation of Telomerase Alternative Splicing: A Target for Chemotherapy).

Researchers have long been convinced that cancer cells can be killed by acting on their telomerases by treating different types of tumors with inhibitors of these enzymes. In combination with surgical and chemotherapeutic methods, antibody-based drugs could revolutionize oncology, but it has not yet reached clinical trials. In order to disable only telomerase and only in tumors (and, for example, not in stem cells) and at the same time not damage healthy cells, a safe ultra-precise tool is needed. Perhaps this particular regulatory site for splicing, which researchers have discovered, will be the key to managing telomerases.

Prepared based on the materials of Medical Xpress: Researchers identify a new potential target for cancer therapy.

Portal "Eternal youth" http://vechnayamolodost.ru 23.04.2013