Regarding cellular self-destruction?

Question

I heard and read telomere 'health' or 'length' ( if that's right ) has alot to do with cell 'health'. If telomere 'abilities' are 'restored' to a 'healthier' status then the cell it is in functions as though it were 'younger'. I was wondering since cancer cells grow without limit and 'older' cells or unstable cells grow with less ferver do cancer cells have functioning telomeres within them and would they somehow be alot more 'robust' then telomeres in normal cells? If this is true could telomeres from cancer cells somehow revitalize the telomeres in normal cells?

Answer 1

First, let's start off with some background. Telomeres are made of DNA and are at the ends of our linear chromosomes. You can think of them as "slack" in the DNA to compensate for the shortening that occurs during DNA replication. Telomerase is the enzyme that makes telomeres (or extends them). As a normal functioning human, telomerase is only functional during development, but after that, telomerase function essentially stops. Therefore you can think of the length of our telomeres as a fuse that will shrink each time the DNA is replicated. Almost like a ticking time bomb to cellular senescence. In simple terms, telomere length can be a marker of how many more divisions a cell can do -- almost like a "lifespan" marker. So you'd think that activating telomerase in adult humans and extending their telomeres would be the cure for aging, right? Not necessarily. In cancer cells, telomerase activity is activated and results in much longer telomeres which are "needed" in order for the cancer cells to divide indefinitely. This, among other reasons, is why cancer cells are immortal. So yes, cancer cells are more robust and often have much longer telomeres than normal aged cells, but that is not to say that they are "healthier." There is some ongoing research regarding the connection of activating telomerase in healthy aging cells to extend their "lifespan." Feel free to read about some of the findings here: https://www.sciencedirect.com/science/article/pii/S0955067417300509

https://www.sciencedirect.com/science/article/pii/B9780128119594000067

But as far as cancerous telomeres "jumping into" aging cells to make them more robust, (a) I don't think this would happen in the first place (DNA is quite large and rarely, if ever, leaves the nucleus, let alone cutting off it's own telomeres and having them absorbed by neighboring cells), and (b) even if it did, I don't imagine it would be protective in the new cell to combat aging as extra DNA often results in disease rather than therapy.

Hope this helps!