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Related Experiment Videos

Tweak induces mammary epithelial branching morphogenesis.

Jennifer S Michaelson1, Sandy Cho, Beth Browning

  • 1Department of Exploratory Science, Biogen Idec, 12 Cambridge Center, Bio6-320, Cambridge MA, USA. Jennifer.Michaelson@BiogenIdec.com

Oncogene
|March 1, 2005
PubMed
Summary

Tumor necrosis factor-related weak inducer of apoptosis (Tweak) promotes mammary gland cancer development by increasing cell proliferation and invasion. Tweak signaling through its receptor Fn14 may drive human breast cancer progression.

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Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Members of the tumor necrosis factor (TNF) superfamily are crucial regulators of cell survival, proliferation, and cancer.
  • Tumor necrosis factor-related weak inducer of apoptosis (Tweak) exhibits diverse biological activities, including proapoptotic, proangiogenic, and proinflammatory functions.

Purpose of the Study:

  • To investigate the role of Tweak in mammary gland transformation using a three-dimensional (3D) cell culture model.
  • To elucidate the molecular mechanisms by which Tweak influences mammary epithelial cell behavior.

Main Methods:

  • Utilized a 3D matrigel culture system with Eph4 mammary epithelial cells.
  • Assessed cell proliferation, invasion, differentiation, and matrix metalloproteinase-9 (MMP-9) levels following Tweak treatment.

Related Experiment Videos

  • Examined the expression of the Tweak receptor, Fn14, in human breast tumor samples and models.

    • Main Results:

    • Tweak treatment induced a branching morphogenic phenotype in mammary epithelial cells, mimicking pro-oncogenic factor effects.
    • Tweak significantly increased cell proliferation and invasiveness while inhibiting functional differentiation.
    • Tweak elevated matrix metalloproteinase-9 (MMP-9) levels, and MMP inhibitors blocked the Tweak-induced branching.
    • Elevated Fn14 protein levels were observed in human breast tumor cell lines, xenografts, and primary tumors.

    Conclusions:

    • Tweak promotes mammary gland tumorigenesis by stimulating proliferation, inhibiting differentiation, and inducing invasion.
    • The Tweak/Fn14 pathway appears to be protumorigenic in human breast cancer, suggesting it as a potential therapeutic target.