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Related Concept Videos

  • Biomedical And Clinical Sciences
  • Oncology And Carcinogenesis
  • Predictive And Prognostic Markers
  • Scrib Expression Is Deregulated In Human Prostate Cancer, And Its Deficiency In Mice Promotes Prostate Neoplasia.
  • Biomedical And Clinical Sciences
  • Oncology And Carcinogenesis
  • Predictive And Prognostic Markers
  • Scrib Expression Is Deregulated In Human Prostate Cancer, And Its Deficiency In Mice Promotes Prostate Neoplasia.

    • Related Experiment Videos

    SCRIB expression is deregulated in human prostate cancer, and its deficiency in mice promotes prostate neoplasia.

    Helen B Pearson1, Pedro A Perez-Mancera, Lukas E Dow

    • 1Cell Cycle and Cancer Genetics Laboratory, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia.

    The Journal of Clinical Investigation
    |October 4, 2011

    View abstract on PubMed

    Summary
    This summary is machine-generated.

    Loss of Scrib, a key polarity regulator, drives prostate cancer in mice by disrupting cellular homeostasis and activating the MAPK cascade. This finding highlights the polarity network as a potential target for prostate cancer therapies.

    Related Experiment Videos

    Area of Science:

    • Oncology
    • Cell Biology
    • Molecular Biology

    Background:

    • Loss of cellular polarity is a hallmark of epithelial cancers.
    • The Scribble complex is crucial for maintaining epithelial polarity.
    • SCRIB, a Scribble complex member, is deregulated in various human cancers.

    Purpose of the Study:

    • To investigate the role of Scrib in prostate homeostasis and tumorigenesis.
    • To elucidate the mechanisms by which Scrib loss contributes to prostate cancer.
    • To assess the clinical relevance of SCRIB deregulation in human prostate cancer.

    Main Methods:

    • Utilized genetically engineered mouse models with targeted Scrib loss.
    • Investigated the effects of Scrib heterozygosity and biallelic loss on prostate tissue.
    • Examined the interplay between Scrib loss, oncogenic Kras, and prostate cancer progression.
    • Analyzed SCRIB expression and its correlation with patient survival in human prostate cancer cohorts.

    Main Results:

    • Scrib is essential for prostate homeostasis in mice.
    • Scrib heterozygosity led to prostate hyperplasia; biallelic loss caused prostate intraepithelial neoplasia.
    • Scrib negatively regulates the MAPK cascade, suppressing tumorigenesis.
    • Combined Scrib loss and oncogenic Kras accelerated prostate cancer progression, mimicking human disease.
    • SCRIB deregulation strongly correlates with poor survival in human prostate cancer patients.

    Conclusions:

    • Scrib plays a critical role in suppressing prostate tumorigenesis.
    • The Scribble polarity network is a potential therapeutic target for prostate cancer.
    • SCRIB deregulation serves as a prognostic marker for poor survival in prostate cancer.