Therapeutic strategy with p53 induces cancer cell death

How U.S. Researchers Focus p53the most frequently mutated tumor suppressor gene, can be activated against cancer cells.

Researcher at the University of Colorado (CU) Anschutz Medical Campusstudy mutations in , USA tumor suppressor gene have a great deal of focus on p53 in human cancer.

Over the past two decades, much effort has been devoted to designing specifically activating biologically targeted therapies. p53However, while these treatments are effective in inducing p53 Due to their activity, they generally cannot kill cancer cells.

New research reveals mechanism of action to prevent p53 Activated from activation effect activation cancer cell deathResearchers have shown that it inhibits two different repressors p53 Cancer cell death can be induced through the activation of a complementary gene network known as the integrated stress response.

Cancer is a disease caused by genetic mutations. These mutated genes in cancer fall into two main categories: tumor suppressors and oncogenes.

“If you block both majors, p53 known as the repressor MDM2and its minor repressor, PPM1D, p53 It works much better at inducing cancer cell death, and this enhanced killing activity requires an integrated stress response,” explained Dr. Joaquín Espinosa, professor of pharmacology at CU School of Medicine.

Research has worked to understand the role of MDM2 and PPM1Dtwo proteins that inhibit p53 Inside tumor cells and the mechanisms that lead to cancer cell death by inhibiting them. “It was already established MDM2 is a major repressor and PPM1D It’s a minor one,” Espinosa explained.

The team then turned to mild oppressors such as: PPM1D so little known PPM1D and other minor repressors p53It quickly became apparent that it inhibited both MDM2 and PPM1D, p53 It can effectively induce cancer cell death.

impede MDM2 and PPM1D It activated the integrated stress response, a signaling pathway that stimulates a protein called ATF4.The researchers also found that ATF4 p53cooperate to cause cancer cell death.

Scientists continue to work to better understand the mechanisms of synergistic reactions that occur when: MDM2 and PPM1D hampered, p53 is enabled. “Our data show that cancer cells are particularly vulnerable to this dual activation. p53 The integrated stress response provides a therapeutic window in the clinic and protects normal cells from killing effects. p53explained Dr. Zdenek Andrysik, assistant professor of pharmacology at the CU School of Medicine.

Espinosa added: p53 Activity to induce tumor regression. The more we learn about the genes and proteins that are mutated in cancer, the more clearly we can tell when the brakes fail and recover, or when the gas pedal goes all the way to the floor and lifts it with a specific targeted inhibitor. you will be able to comprehend. “

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