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Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
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Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

Transcriptional regulation of human survivin by early growth response (Egr)-1 transcription factor

Mandy Wagner1, Karin Schmelz, Bernd Dörken

  • 1Department of Hematology and Oncology, Universitätsmedizin Berlin, Charité, Campus Virchow, Augustenburger Platz 1, 13353 Berlin, Germany.

International Journal of Cancer
|November 22, 2007
PubMed

Insights

This study identifies a new way to control survivin, a protein linked to cancer cell division and survival. The early growth response 1 (Egr-1) transcription factor can reduce survivin levels, potentially making cancer cells more vulnerable to apoptosis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Survivin, an inhibitor of apoptosis protein, is crucial for cell division and survival.
  • Its tumor-specific expression makes survivin a promising therapeutic target for malignant diseases.
  • Understanding survivin's transcriptional regulation is key for developing new anti-cancer strategies.

Purpose of the Study:

  • To investigate the transcriptional regulation of survivin.
  • To identify novel regulatory regions within the survivin promoter.
  • To establish survivin as a target gene for novel therapeutic approaches.

Main Methods:

  • Analysis of the human survivin promoter region.
  • Treatment with phorbol 12-myristate-13-acetate to induce Egr-1.
  • In vitro and in cellulo binding assays for Egr-1 to the survivin promoter.
  • Reporter-gene assays and overexpression experiments.
  • Utilizing p53 wildtype and mutated cell lines.

Main Results:

  • A novel regulatory region in the survivin promoter was identified.
  • The early growth response 1 (Egr-1) transcription factor binds to a specific sequence (5'GAGGGGGCG 3') in the survivin promoter.
  • Exogenous expression of wildtype Egr-1 downregulates survivin expression.
  • Egr-1 negatively regulates survivin expression and sensitizes cells to TRAIL-induced apoptosis, particularly in p53 wildtype cells.

Conclusions:

  • Egr-1 acts as a negative regulator of survivin expression.
  • The Egr-1/survivin pathway offers a potential new therapeutic strategy for cancer treatment.
  • Targeting Egr-1 could enhance apoptosis in tumor cells, leading to improved treatment outcomes.

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