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Related Experiment Videos

Oncogenes induce and activate endogenous p73 protein.

A Zaika1, M Irwin, C Sansome

  • 1Department of Pathology, State University of New York at Stony Brook, Stony Brook, New York 11794-8691, USA.

The Journal of Biological Chemistry
|December 25, 2000
PubMed
Summary

Oncogenes like E2F1, c-Myc, and E1A activate the TP73 gene in p53-deficient tumor cells. This activation triggers apoptosis, suggesting TP73

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Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Understanding upstream pathways for TP73 is vital for its biological role.
  • TP73 may be involved in tumorigenesis.
  • Investigating oncogene influence on TP73 is necessary.

Purpose of the Study:

  • To determine if oncogenes can induce and activate endogenous TP73.
  • To explore TP73's role in oncogene-induced apoptosis in p53-deficient cells.

Main Methods:

  • Overexpression of E2F1, c-Myc, and E1A in p53-deficient tumor cells.
  • Assessing p73 protein levels and transcriptional activity.
  • Evaluating apoptosis induction and inhibition using p73 dominant-negative constructs.

Main Results:

  • E2F1, c-Myc, and E1A up-regulate endogenous p73 alpha and beta proteins.
  • Activated p73 drives transcription of target genes (p21, HDM2) and induces apoptosis.
  • Inhibiting p73 blocks oncogene-induced apoptosis in SaOs-2 cells.

Conclusions:

  • Oncogenes signal to TP73 in vivo.
  • In p53-deficient tumors, oncogenes can utilize TP73 to induce apoptosis.

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