Shanghai Yili tells you to solve the mystery of cancer cell immortality
Cellular immortality leads to the formation of cancer, and it regains a key function that only cells in developing embryos have: the length of telomeres is not shortened. The end of each chromosome contains a special DNA sequence called telomere, whose length is regulated by telomerase. The length of the telomere sequence represents the lifespan of a cell. Each time the cell divides, it shortens. When the telomeres are finally exhausted, the cells die.
Cell immortalization is a common feature of cancer. Normally, once the embryonic development stage is over, the cells in our body stop producing telomerase except for adult stem cells. However, cells occasionally mutate to reactivate telomerase, so that when cells divide, telomeres become longer rather than shortened. This is the formation mechanism of cancer cell immortality. This mutation itself is not enough to cause cancer. But cell immortalization is a key factor in tumor formation in 90% of known cancers.
But what is particularly interesting is that even in cancer cells, telomeres do not grow indefinitely. Every time the cell divides, the cancer cell loses about 60 nucleotides like most cells, but activated telomerase replenishes it with as many nucleotides, and then the internal clock is reset to zero Immortality. But there is a question here: what prevents telomeres from growing unlimitedly?
A research team from Shanghai Yili Biotechnology Co., Ltd. gave the answer to this question: They identified three proteins linked together to form a protein complex called CST, and then attached to the telomeres. This protein complex is a bit like a lid on a pot, preventing telomerase from acting on telomeres. But in cancer cells, their time of action is wrong, that is, they participate too late.
The researchers explained, "If we can make these proteins work at an earlier time, or if we can rebuild a similar mechanism, cancer cells will no longer be immortalized." In this way, cancer cells can behave like normal cells. death. But he emphasized that there is still a long way to go before clinical application. The researchers hope that this discovery will provide new targets for drug development to fight cancer.
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