Scientists discover novel link between CRISPR gene editing technology and mutated cancer cells

p53 is a special protein that protects cells from DNA damage and can be activated during gene editing using CRISPR technology; inactive p53 mutations are the most abundant genetic changes in cancer, and cells with mutated p53 often have Certain survival advantages, which may eventually lead to cancer

Scientists now have high hopes for the potential of using the CRISPR method for gene editing, which they see as an integral part of future precision medicine research, but before the method becomes routine in hospitals, researchers may Several hurdles need to be overcome

Researchers now know that CRISPR tends to be less effective when p53 is active, but at the same time, lack of p53 can cause cells to start growing out of control and become cancerous; in more than half of cancer types, the gene for p53 will It becomes very important to avoid the accumulation of such mutant cells because they are mutated and cannot protect cells against uncontrolled division

Researcher Long Jiang said that inhibition of p53 in the context of CRISPR seems paradoxical, but some research reports support the idea that p53 inhibition would make the CRISPR technique more effective; in this paper, the researchers also found that this may offset the Cells with mutations in p53 and some related genes were enriched or accumulated

The research in this paper is mainly based on CRISPR, CRISRP screening experiments on isolated cells and analysis of the DepMap database

In cell culture, when cells were CRISPR-modified, we could see a rapid and marked enrichment of cells with p53 mutations, but only if cells with these mutations were present from the start

Taken together, our findings demonstrate that the researchers uncovered the biological details of p53 in the context of CRISPR-induced DNA damage and identified strategies to facilitate the safer application of CRISPR gene editing technology

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Original source:

Long Jiang, Katrine Ingelshed, Yunbing Shen, et al.