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Related Experiment Video

Updated: Jun 21, 2026

A Unified Methodological Framework for Vestibular Schwannoma Research
08:43

A Unified Methodological Framework for Vestibular Schwannoma Research

Published on: June 20, 2017

p73 expression and function in vestibular schwannoma.

Zana K Ahmad1, Xabier Altuna, Jay Patrick Lopez

  • 1Division of Otolaryngology-Head and Neck Surgery, Department of Surgery, University of California, San Diego, La Jolla, CA 92093-0612, USA.

Archives of Otolaryngology--Head & Neck Surgery
|July 22, 2009
PubMed
Summary
This summary is machine-generated.

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The tumor suppressor p73 is expressed in some vestibular schwannomas (VS). Its forced expression induces apoptosis and sensitizes VS cells to radiation, suggesting potential gene therapy applications.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Vestibular schwannoma (VS) is a tumor affecting the nerve connecting the ear to the brain.
  • The p53 family member p73 is a tumor suppressor with roles in cell cycle regulation and apoptosis.
  • Understanding p73's role in VS is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate p73 expression in vestibular schwannoma (VS) tissues.
  • To assess the functional role of p73 in regulating the proliferation and apoptosis of a human papillomavirus E6-E7 immortalized VS cell line (HEI193).

Main Methods:

  • Immunohistochemistry, Western blot, and immunofluorescence were used to detect p73 expression in VS tissues and HEI193 cells.
  • HEI193 cells were transfected with p73 to analyze cell cycle distribution, apoptosis, and necrosis using flow cytometry, annexin V, and TUNEL assays.

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Last Updated: Jun 21, 2026

A Unified Methodological Framework for Vestibular Schwannoma Research
08:43

A Unified Methodological Framework for Vestibular Schwannoma Research

Published on: June 20, 2017

Primary Culture of Human Vestibular Schwannomas
10:50

Primary Culture of Human Vestibular Schwannomas

Published on: July 20, 2014

  • The impact of p73 on ionizing radiation-induced cell death was evaluated.

    • Main Results:

    • p73 was expressed in 41% of 34 VS tissues but not in HEI193 cells.
    • Forced p73 expression in HEI193 cells induced G1 cell cycle arrest, increased p21 levels, and promoted apoptosis and necrosis.
    • p73 expression significantly enhanced radiation-induced apoptosis and necrosis in HEI193 cells.

    Conclusions:

    • p73 acts as a tumor suppressor in VS by inducing apoptosis and cell cycle arrest.
    • Forced p73 expression may offer therapeutic strategies for VS, either directly inducing apoptosis or sensitizing tumors to radiation therapy.