Could Eliminating Telomere-Protecting Mechanisms Increase the Power of Chemotherapy?

The specialized sections at the ends of our chromosomes that determine how long a cell will divide are called telomeres . The relationship of telomeres with aging and cancer has been studied for many years. Research at the Salk Institute discovered that telomeres have an important role in programmed cell death and that this prevents tumor formation.
Our cells multiply by dividing, and this process is called mitosis . With every division, the cells' telomeres shorten. Eventually, telomere length reaches a critical level and cell division stops. This is a natural barrier against cancer. It prevents cells with unstable or damaged genetic structures from multiplying. Cancer cells easily overcome this barrier and continue dividing because they develop a mechanism to protect their telomeres. According to the research team, the longer cell division takes, the closer the cell comes to crisis and programmed cell death. Normal mitosis lasts 30-45 minutes, and when this exceeds 2 hours, cells begin to enter crisis. During this natural crisis period, the protein protecting the cell's telomeres becomes inactive, sends a DNA damage signal, and cells begin to break themselves down. In this study, cells were imaged in real time to observe their division. Cells with prolonged mitosis were observed to enter crisis, lose their telomere-protecting proteins, and initiate the program that would break them down.
Paclitaxel and similar drugs target mitosis to stop cancer. The researchers hypothesize that preventing telomere protection could increase the effects of mitotic inhibitors such as taxol. Understanding the role of telomeres in cell death could also pave the way for next-generation treatments.
This study was published in Nature, one of the world's most prestigious scientific journals, on 24 June 2015. For more detailed information, you can consult the article in the references section.
Sources
Cell death during crisis is mediated by mitotic telomere deprotection.
Nature, 2015
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