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Related Experiment Video

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Yeast As a Chassis for Developing Functional Assays to Study Human P53
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Mutant p53 inhibits miRNA biogenesis by interfering with the microprocessor complex.

F Garibaldi1, E Falcone1, D Trisciuoglio1

  • 1Department of Research, Advanced Diagnostics, and Technological Innovation, Translational Research Area, Regina Elena National Cancer Institute, Rome, Italy.

Oncogene
|March 22, 2016
PubMed
Summary
This summary is machine-generated.

Mutant p53 (mutp53) oncoproteins disrupt microRNA (miRNA) biogenesis in cancer by sequestering RNA helicases. This leads to decreased mature miRNA levels and promotes tumor suppressor roles for these miRNAs.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • MicroRNAs (miRNAs) are often downregulated in cancers, suggesting tumor suppressor functions.
  • The mechanisms regulating miRNAs in cancer and their link to oncogenes are not fully understood.
  • Mutations in the TP53 gene create mutant p53 (mutp53) oncoproteins with gain-of-function activities.

Purpose of the Study:

  • To investigate how mutant p53 (mutp53) oncoproteins affect microRNA (miRNA) biogenesis in cancer.
  • To elucidate the molecular mechanisms underlying miRNA deregulation by mutp53.
  • To determine the functional significance of mutp53-modulated miRNAs in tumorigenesis.

Main Methods:

  • Confocal microscopy, co-immunoprecipitation, and RNA-chromatin immunoprecipitation were used to study protein-RNA interactions.
  • Assays were performed to assess the impact of p72 overexpression on mature miRNA levels.
  • Functional experiments were conducted to evaluate the tumor-suppressive roles of specific miRNAs.

Main Results:

  • Mutant p53 (mutp53) oncoproteins inhibit the post-transcriptional maturation of a subset of microRNAs (miRNAs) in cancer cells.
  • Endogenous mutp53 binds and sequesters RNA helicases p72/82 from the microprocessor complex, disrupting Drosha-pri-miRNA association.
  • Overexpression of p72 increased mature miRNA levels, and several mutp53-downregulated miRNAs exhibited tumor-suppressive functions.

Conclusions:

  • Mutant p53 (mutp53) interferes with Drosha-p72/82 association, representing a novel mechanism for miRNA deregulation in cancer.
  • This interference contributes to the reduced levels of tumor-suppressive miRNAs observed in various human cancers.
  • Targeting this mutp53-mediated pathway could offer new therapeutic strategies for cancer treatment.