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Negative cross talk between NFAT1 and Stat5 signaling in breast cancer

Jiamao Zheng1, Feng Fang, Xianke Zeng

  • 1Women’s Cancer Research Program, Robert H. Lurie Comprehensive Cancer Center & Department of Pathology, Northwestern University, Chicago, Illinois 60611, USA.

Molecular Endocrinology (Baltimore, Md.)
|October 4, 2011
PubMed

Insights

The calcineurin/nuclear factor of activated T cells (NFAT) pathway inhibits signal transducers and activators of transcription 5 (Stat5) in breast cancer. This reciprocal antagonism impacts tumor growth and metastasis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • The molecular mechanisms regulating Signal Transducers and Activators of Transcription 5 (Stat5) in breast cancer progression are not fully understood.
  • Stat5 plays a critical role in breast cancer development and metastasis.

Purpose of the Study:

  • To elucidate the molecular mechanisms governing Stat5 activity during breast cancer progression.
  • To investigate the interplay between the calcineurin/nuclear factor of activated T cells (NFAT) pathway and Stat5 signaling in breast cancer.

Main Methods:

  • Co-immunoprecipitation assays to detect protein-protein interactions.
  • Western blotting to assess protein activation and expression.
  • RNA interference (RNAi) to silence NFAT1.
  • Quantitative real-time PCR to measure gene expression.
  • Analysis of breast cancer tissue microarrays.

Main Results:

  • NFAT1 physically interacts with Stat5 in breast cancer cells.
  • NFAT1 inhibits Stat5-dependent transactivation, gene expression, and promoter binding.
  • Silencing NFAT1 enhances Stat5-mediated gene transcription and breast cancer cell proliferation.
  • Stat5 activity reciprocally inhibits NFAT1 signaling.
  • A negative correlation exists between NFAT1 and activated Stat5 (pY694) levels during breast cancer progression.

Conclusions:

  • A novel negative cross-talk exists between NFAT1 and Stat5 signaling pathways in breast cancer.
  • This antagonistic interaction influences breast tumor formation, growth, and metastasis.

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