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Related Experiment Videos

Quantitative TP73 transcript analysis in hepatocellular carcinomas.

Thorsten Stiewe1, Sebastian Tuve, Martin Peter

  • 1Center for Cancer Research and Cancer Therapy, Institute of Molecular Biology, University of Essen Medical School, Essen, Germany.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|February 5, 2004
PubMed
Summary

The study found that aberrant splicing of p73 transcripts from the TA promoter, not alternative promoter usage, drives overexpression of oncogenic DeltaTA-p73 isoforms in hepatocellular carcinoma. This suggests the TA promoter

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • The p53 family member p73 has homology to p53, but its role in cancer is complex.
  • Two main classes of p73 isoforms exist: full-length, transactivation-competent TA-p73 (putative tumor suppressor) and NH(2)-terminally truncated, transactivation-deficient DeltaTA-p73 (oncogenic).
  • Oncogenic DeltaTA-p73 isoforms can arise from aberrant splicing or alternative promoter usage (DeltaN-p73).

Purpose of the Study:

  • To investigate the origin of oncogenic DeltaTA-p73 isoforms in hepatocellular carcinoma (HCC).
  • To determine whether aberrant splicing or alternative promoter usage is responsible for elevated DeltaTA-p73 levels in HCC.

Main Methods:

  • Quantification of p73 transcripts from 10 HCC patient samples.
  • Utilized isoform-specific real-time reverse transcription-PCR to analyze p73 transcript levels.

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  • Differentiated between transcripts originating from the TA promoter (including aberrantly spliced forms) and the DeltaN promoter.

    • Main Results:

    • Aberrantly spliced DeltaTA-p73 transcripts originating from the TA promoter showed significantly increased expression in HCC tumors.
    • DeltaN-p73 transcripts, generated from the alternative intronic promoter, were not significantly up-regulated in the analyzed HCC samples.

    Conclusions:

    • The findings suggest that elevated activity of the TA promoter is the primary driver for high-level expression of both full-length TA-p73 and oncogenic DeltaTA-p73 isoforms in HCC.
    • Aberrant splicing of TA-p73 transcripts, rather than alternative promoter usage, is the main mechanism contributing to the oncogenic p73 isoform pool in hepatocellular carcinoma.