CRISPR-Cas9 works by creating double-stranded DNA breaks at specific points in a DNA sequence, allowing scientists to target and edit specific genes. However, the p53 gene responds to double-stranded breaks by arresting cell growth, meaning that cells that have undergone CRISPR would grow and divide less effectively. This means that cells with mutations in the p53 gene can continue to grow and divide normally, giving them a competitive advantage.
The p53 gene stops cell division if a genomic error arises and attempts to correct the problem. If the error cannot be fixed, p53 will initiate programmed cell death before the cells can become cancerous. This makes p53 a critical anti-cancer gene and losing its function can make people more susceptible to tumors.
Computational biologists… analyzed p53 responses to double-stranded breaks in nearly 1,000 human cell lines.
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In almost every cell type, they found that after CRISPR-Cas9 KO, cells with normal p53 genes exhibited slower growth, while those with mutated p53 genes were less affected, allowing them to grow faster and outcompete the normal cells.
They also found that CRISPR may confer an advantage to cells with other cancer-associated mutations, like those of the KRAS oncogene.
