Abstract:
This article shares industry information from Guangzhou Jennio Biotech, covering breakthroughs like a CRISPR-p53 mutation link in cancer, AI-enhanced microscopes for 3D biological imaging, HBV’s role in liver cell chromosomal changes and hepatocellular carcinoma, E. coli growth burden mechanisms via Cra transcription factor dysregulation, intelligent anti-tumor nano-drugs for targeted vascular embolization, and the lymphoma drug Monjuvi+lenalidomide for DLBCL therapy.
Details:
p53, a special protein that protects cells from DNA damage, is activated during gene editing using CRISPR technology; inactivating p53 mutations are the most abundant genetic alterations in cancer, and cells carrying mutated p53 often have A certain survival advantage, which may eventually lead to cancer. Recently, a research report titled “CRISPR/Cas9-induced DNA damage enriches for mutations in a p53-linked interactome: implications for CRISPR-based therapies” published in the international journal Cancer Research, from Karolinska Institutet, Sweden, etc. Scientists at the agency discovered a novel link between CRISPR, p53 and other cancer genes through research, which may be effective in preventing the accumulation of mutant cells without affecting the effectiveness of “genetic magic shear”.
Scientists are now pinning great hopes on the potential of using the CRISPR method for gene editing, which they see as an integral part of future precision medicine research. Several hurdles need to be overcome. One of the challenges is how a cell’s behavior changes when it is subjected to DNA damage. CRISPR gene editing tends to cause this damage in a controlled way, and the damage to the cell activates the p53 protein, which acts as a “First aid response” to DNA damage.
Researchers now know that CRISPR tends to be less effective when p53 is active, but at the same time, a lack of p53 can cause cells to start growing out of control and becoming cancerous; in more than half of all cancer types, the gene for p53 Mutated and unable to protect cells against uncontrolled division, it becomes important to avoid the accumulation of such mutant cells. Here, the researchers show that when CRISPR is applied, cells carrying p53-inactivating mutations gain a survival advantage that also accumulates in mixed cell populations. In addition, the researchers identified a specific network that links genes with mutations that have similar effects on p53 mutations, and they found that transiently inhibiting p53 may be a possible pharmacological strategy to prevent Cells carrying such mutations are enriched.
Researcher Long Jiang said that inhibiting p53 in the context of CRISPR seems to be contradictory, but some research reports support the idea that the inhibition of p53 will make CRISRP technology more effective; in this paper, the researchers also found that this may be able to counteract Cells with mutations in p53 and some related genes were enriched or accumulated. This study has a certain role in promoting the clinical application of CRISPR technology in the future, because the researchers have identified a possible candidate gene network. When applying CRISPR technology to cells, it is necessary to strictly control the mutations in cells. Another possible conclusion is that transient inhibition of p53 may serve as a novel strategy to reduce the enrichment of mutant cells. The researchers also point out that the DNA damage response may serve as a marker for the possibility of developing more precise guide RNA sequences that could be used to reveal the sites in the DNA sequence that CRISPR is intended to alter.
This study is mainly based on CRISPR, CRISRP screening experiments on isolated cells and analysis of the DepMap database. Next steps for the researchers will be to delve deeper into understanding just how connected the described mechanisms are.
In cell culture, when cells are modified with CRISPR, we can see a rapid and significant enrichment of cells with p53 mutations, but only if cells with these mutations are present from the beginning. So at the moment researchers can demonstrate the existence of the mechanism and the factors that affect it, but they don’t know to what extent this is a real problem, which may be what the researchers hope will need to be explored further in more clinical center tests The problem.
Taken together, our findings demonstrate that researchers have uncovered biological details of p53 in the context of CRISPR-induced DNA damage, while also identifying strategies that could facilitate the safer application of CRISPR gene-editing technology.
