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Functional properties of WT1

D A Haber¹, C Englert, S Maheswaran

¹Harvard Medical School, Charlestown, Massachusetts.

Medical and Pediatric Oncology

|November 1, 1996

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The WT1 gene, a tumor suppressor, induces programmed cell death in embryonal cancer cells. This apoptosis is linked to the repression of epidermal growth factor receptor (EGFR) and is independent of p53.

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

WT1 (Wilms' Tumor 1) is a zinc finger transcription factor.
WT1 inactivation is observed in a subset of Wilms' tumors.
WT1 functions as a tumor suppressor gene, inhibiting growth in certain cancer cells.

Purpose of the Study:

To further characterize the functional properties of WT1.
To investigate WT1's role in programmed cell death in embryonal tumor cells.
To identify downstream targets of WT1-mediated apoptosis.

Main Methods:

Established U2OS and Saos-2 cell lines expressing WT1 variants under a tetracycline-repressible promoter.
Induced WT1 expression and assessed cell death.
Analyzed transcriptional repression of epidermal growth factor receptor (EGFR).

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Main Results:

WT1 induction triggered programmed cell death (apoptosis) in embryonal cancer cells.
Apoptosis was mediated by WT1 isoform B and was p53-independent.
WT1 repressed EGFR transcription and reduced EGFR protein synthesis.
Constitutive EGFR expression blocked WT1-induced cell death.

Conclusions:

Wild-type WT1 induces apoptosis in embryonal cancer cells.
WT1 likely functions by withdrawing growth factor survival signals.
EGFR is a physiological target gene of WT1.