Cancer Advocate
Telomerase can protect cancer cells
Polina Gershberg, Naked Science
New data on how the enzyme telomerase protects the DNA of cancer cells should help in the development of more effective cancer treatments. An article about this was published in the journal Science Advances (Perera et al., Telomerase promotes formation of a telomere protective complex in cancer cells).
Somatic cells of the human body naturally stop dividing after a certain number of cycles – the so-called Hayflick limit. With each division in the DNA of the cell, the end sections – telomeres - are reduced, which at some point makes it impossible to replicate the genetic material.
Cancer cells can divide almost indefinitely – this is provided by telomerases, enzymes that complete telomeres. Suppression of telomerase activity in tumor cells is considered one of the promising directions in the treatment of cancer. This method has its drawbacks: after the final suppression of telomerase activity, cancer cells will undergo many more division cycles before reaching the Hayflick limit.
However, telomere completion is not the only way telomerase keeps cancer cells alive. Australian scientists have discovered that one of its components, hTERT (human telomerase reverse transcriptase, human telomerase reverse transcriptase), induces the launch of mechanisms that maintain the stability of the telomerase itself and the DNA of the cell.
Figure from the article Lü et al. hTERT-based therapy: A universal anticancer approach (Review) // Oncology Reports, 2012 – WM.
The main function of hTERT is reverse transcription. This enzyme is able to synthesize a DNA chain based on an RNA matrix. The removal of hTERT from cancer cells led to a delay in the G1 phase of the cell cycle - in it, cells synthesize matrix RNA and proteins necessary for division. In addition, the removal of hTERT from the cell led to a decrease in the expression of the Apollo protein and heat shock proteins, which play an important role in the stability of DNA in general.
The researchers concluded that hTERT has a previously unidentified important role in the functioning of cancer cells. This enzyme promotes the formation of a telomeric protective complex containing heat shock proteins Hsp70-1 and Apollo protein and is necessary for the stable proliferation of telomerase-positive cells.
Scientists are confident that simultaneous reduction of the catalytic ability of telomerase and suppression of the protective properties of hTERT will accelerate the death of cancer cells. This should contribute to a breakthrough in the creation of drugs against cancer.
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