Modulation of Stat3 Alternative Splicing in Breast Cancer

Abstract

Stat3 is a transcription factor constitutively active in a large number of breast cancers and other tumors, where it works as a central player in the activation of multiple oncogenic pathways. We developed a method to modulate endogenous Stat3 alternative splicing using modified antisense oligonucleotides, to induce the dominant negative Stat3-beta variant in vitro and in vivo. Switching from the full length Stat3 isoform to the stat3-beta variant leads to increased tumor cell death and complete tumor regression in animal models via a novel modulatory mechanism.

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Document Details

Document Type
Technical Report
Publication Date
Sep 01, 2010
Accession Number
ADA549137

Entities

People

  • Luca Cartegni

Organizations

  • Memorial Sloan Kettering Cancer Center

Tags

DTIC Thesaurus Topics

  • Amino Acids
  • Antisense Elements (Genetics)
  • Apoptosis
  • Azo Compounds
  • Biomedical Research
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Cytoplasm
  • Growth Factors
  • Neoplasms
  • Pcr Testing
  • Proteins
  • Sites
  • Standards
  • Transcription Factors

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.