Health
Simultaneous mutation of two nonessential genes can cause cancer cell death
The Ludwig Cancer Research study identifies a new case in which co-mutation of two nonessential genes can cause cancer cell death because neither is itself essential for cell survival.
Published today by Richard Colodner, a member of Ludwig San Diego Minutes of the National Academy of Sciences, The study also shows that this deadly synergistic effect, or “synthetic lethality,” can be replicated by drug-like molecules and used to treat cancer.
Development of a new generation of drugs called PARP inhibitors and the FDA to treat malignancies defective in the tumor suppressor genes BRCA1 and BRCA2 involved in breast cancer, ovarian cancer, and many other types of cancer With the approval, there is considerable interest in exploitation. Synthetic lethal interactions for the development of cancer treatments.
Scientists, including the Corodner group, are exploring other synthetic lethal interactions in cancer. “PARP inhibitors are a big breakthrough, but they are not perfect. Patients can become resistant and there is always a need for newer and better therapies.”
Based on research done in yeast cells, Kolodner et al. found that disabling or deleting FEN1, a mammalian gene important for DNA replication and repair, led to cancer cells with mutated forms of BRCA1 and 2. Found to be harmful to.
We provide data that make people consider FEN1 a potentially interesting therapeutic target, demonstrating how yeast can be used to predict the full range of synthetic lethal interactions, and a true Can be validated with genetic tools in cancer cell lines. “
Richard Corodner, Professor, Department of Cellular and Molecular Medicine, University of California San Diego
In previous studies with yeast Saccharomyces cerevisiae Kolodner and his colleagues have discovered that the RAD27 gene has synthetic lethal interactions with 59 other non-essential yeast genes as a model for identifying and studying genes that support genomic integrity. ..
Two such notable genes are RAD51 and RAD52, which play a role in DNA recombination.
FEN1 is a close counterpart, or homologue, of RAD27 in mammals. Based on yeast studies, Kolodner et al. predicted that FEN1 has a synthetic lethal interaction with BRCA1 and BRCA2. They function in the same biochemical pathways as RAD51 and RAD52 in yeast.
To test this hypothesis, they synthesized four FEN1 blockers and used CRCA to suppress FEN1 activity in cancer cell lines with and without the BRCA mutation. C8 was found to be an effective killer for BRCA mutant cells.
Next, we showed that gene disruption of FEN1 expression had the same effect as C8 on BRCA mutant cells, confirming that C8 functions by inducing synthetic lethality.
Finally, scientists transplanted C8-sensitive and C8-resistant tumors into mice and showed that C8 significantly inhibited the growth of C8-sensitive tumors, but not C8-resistant tumors.
Interestingly, not all cancer cell lines and tumors that responded to C8 treatment were BRCA deficient, indicating that FEN1 has a synthetic lethal interaction with other genes.
These findings identify FEN1 as a new target for drugs to treat various malignancies by inducing synthetic lethality.
They also show that yeast-based screening is a powerful tool to accelerate the discovery of synthetic lethal interactions of potential therapeutic value-an ongoing project at the Corodner Institute.
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