Alk about your work on making cancer cells “more mortal.”
The majority of the cancer cells, about 90 percent, they activate a molecule called telomerase. Telomerase is usually not activated in normal cells, except for in stem cells. In cancer cells, the telomerase is active. The function of telomerase is to add telomere DNA at the short telomeres. That’s why cancer cells don’t lose their telomeres. In the normal cells telomerase is off, so there is no way to maintain their telomere length.
[This would suggest that] if you kill the telomerase in cancer cells, the telomere [would gradually shorten] and the cancer cells will die.
However, recently we have found that the telomerase extends just one strand of DNA. The other strand should be synthesized by other molecules, other proteins. We found the molecule that’s responsible for synthesizing the other strand. If you block the function of this molecule, then the telomere cannot be maintained properly, so the cell also just stops growing.
We’re just at this stage now. We don’t know how this whole thing works. We’re working on that and hopefully in the future we can design a way to target this process, not directly target telomerase but target the synthesis of the other strand. That’s another way of stopping the cancer cell’s growth.
What’s the next step to move this research forward?
The next step will be to find out how this whole thing is regulated. We’d like to know whether in normal cells the synthesis of the other strand also occurs because you want to specifically target the cancer cells. If this does exist, [we want to know] whether the same process is regulated by different pathways in normal cells compared to cancer cells. Our ultimate goal is to see if there are any specific targets we can inhibit in the cancer cells.
The majority of the cancer cells, about 90 percent, they activate a molecule called telomerase. Telomerase is usually not activated in normal cells, except for in stem cells. In cancer cells, the telomerase is active. The function of telomerase is to add telomere DNA at the short telomeres. That’s why cancer cells don’t lose their telomeres. In the normal cells telomerase is off, so there is no way to maintain their telomere length.
[This would suggest that] if you kill the telomerase in cancer cells, the telomere [would gradually shorten] and the cancer cells will die.
However, recently we have found that the telomerase extends just one strand of DNA. The other strand should be synthesized by other molecules, other proteins. We found the molecule that’s responsible for synthesizing the other strand. If you block the function of this molecule, then the telomere cannot be maintained properly, so the cell also just stops growing.
We’re just at this stage now. We don’t know how this whole thing works. We’re working on that and hopefully in the future we can design a way to target this process, not directly target telomerase but target the synthesis of the other strand. That’s another way of stopping the cancer cell’s growth.
What’s the next step to move this research forward?
The next step will be to find out how this whole thing is regulated. We’d like to know whether in normal cells the synthesis of the other strand also occurs because you want to specifically target the cancer cells. If this does exist, [we want to know] whether the same process is regulated by different pathways in normal cells compared to cancer cells. Our ultimate goal is to see if there are any specific targets we can inhibit in the cancer cells.
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