P21, the protein of immortality for cancer cells
The molecule slows the proliferation of tumor cells while giving the time needed to repair the damage to their DNA. The discovery, made by Italian researchers IEA, is published in Nature.
The secret of immortality of cancer stem cells - those that feed it and cause relapses because they're immune to chemotherapy - was unveiled. Their strength is the p21 protein that slows the proliferation, giving them the time needed to repair damage to DNA. In practice, it is as if these cells were able to rejuvenate indefinitely: no age, and thus do not die. By blocking the production of p21, however, you can make them vulnerable and hit the tumor at the root.
The research was conducted in the laboratories of the European Institute of Oncology (IFOM-IEO) in collaboration with the universities of Milan and Perugia, and was published this week in Nature.
The cells age and die because they accumulate damage and mistakes borne of DNA during cell divisions. To understand why this does not happen in a cancerous stem cell, the researchers observed what happens to a staminale "normal" when you alter one of the genes (oncogenes) that cause cancer (in this case, the acute myeloid leukemia).
The study revealed that oncogenes stimulate the activity of another gene, called p21, and thus the production of the corresponding protein, whose effect is to slow the proliferation. In essence, these cells have much more time to repair other damaged DNA, and remain young and active, immune to chemotherapy drugs because they recognize and affect only the cells in rapid proliferation.
The secret of immortality of cancer stem cells - those that feed it and cause relapses because they're immune to chemotherapy - was unveiled. Their strength is the p21 protein that slows the proliferation, giving them the time needed to repair damage to DNA. In practice, it is as if these cells were able to rejuvenate indefinitely: no age, and thus do not die. By blocking the production of p21, however, you can make them vulnerable and hit the tumor at the root.
The research was conducted in the laboratories of the European Institute of Oncology (IFOM-IEO) in collaboration with the universities of Milan and Perugia, and was published this week in Nature.
The cells age and die because they accumulate damage and mistakes borne of DNA during cell divisions. To understand why this does not happen in a cancerous stem cell, the researchers observed what happens to a staminale "normal" when you alter one of the genes (oncogenes) that cause cancer (in this case, the acute myeloid leukemia).
The study revealed that oncogenes stimulate the activity of another gene, called p21, and thus the production of the corresponding protein, whose effect is to slow the proliferation. In essence, these cells have much more time to repair other damaged DNA, and remain young and active, immune to chemotherapy drugs because they recognize and affect only the cells in rapid proliferation.
Silence the gene p21, however, the cancer stem cells begin to accumulate damage to the DNA, and then grow old and die. "Our discovery," said Pier Giuseppe Pelicci, scientific director of the Department of Experimental Oncology IEA and coordinator of the study, "shows a way to eliminate the cancer stem cells: their systems to block the repair of the genome. New drugs that inhibit the shelter of the genome are taking the first steps of clinical trials in human beings. We will know in the next five or ten years if they are effective in treating cancer.
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That's amazing!
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