Loss of the Par3 Polarity Protein Promotes Breast Tumorigenesis and Metastasis

Abstract

(Cancer Cell 22, 601–614; November 13, 2012) During figure preparation for this article, the authors inadvertently duplicated control tubulin blots in Figure 5D and Figure 5E. The authors regret this error and apologize for any confusion that it may have caused. These errors have now been corrected in the figure below. Loss of the Par3 Polarity Protein Promotes Breast Tumorigenesis and MetastasisMcCaffrey et al.Cancer CellNovember 13, 2012In BriefLoss of epithelial organization is a hallmark of carcinomas, but whether polarity regulates tumor growth and metastasis is poorly understood. To address this issue, we depleted the Par3 polarity gene by RNAi in combination with oncogenic Notch or Ras61L expression in the murine mammary gland. Par3 silencing dramatically reduced tumor latency in both models and produced invasive and metastatic tumors that retained epithelial marker expression. Par3 depletion was associated with induction of MMP9, destruction of the extracellular matrix, and invasion, all mediated by atypical PKC-dependant JAK/Stat3 activation. Full-Text PDF Open Archive