Loss of wild-type p53 promotes mutant p53-driven metastasis through acquisition of survival and tumor-initiating properties
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For mutant forms of a tumor suppressor to drive the spread of cancer, cancer cells must also lose their second working copy of the protein. This finding could lead to new treatment strategies.
Many cancers are driven by mutations in specific genes. Inactivation of the p53 tumor suppressor is the most common alteration in human cancer.
A Kanazawa University–led team showed in mice that the loss of the second p53 is necessary for dormant cancer cells to survive and then seed new tumors once they have migrated to other sites in the body.
Inflammatory and growth factor pathways become activated in these cells, along with an acquisition of stem cell properties. Together, these molecular changes enhance the tumour-initiating abilities of cells in which one p53 is mutant and the other p53 is deleted.
The researchers propose that therapeutically blocking p53 loss could thus help stop the movement of cancer cells from one tissue to another.
- Nature Communications 11, 2333 (2020). doi: 10.1038/s41467-020-16245-1
|Kanazawa University (KU), Japan||0.67|
|Theragen Etex Bio Institute, South Korea||0.22|
|Advanced Institutes of Convergence Technology (AICT), SNU, South Korea||0.06|
|Seoul National University (SNU), South Korea||0.06|