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首页> 外文期刊>Cancer Cell >Loss of the Par3 Polarity Protein Promotes Breast Tumorigenesis and Metastasis
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Loss of the Par3 Polarity Protein Promotes Breast Tumorigenesis and Metastasis

机译：Par3极性蛋白的丢失会促进乳腺癌的发生和转移。

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Loss 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. Importantly, Par3 expression is significantly reduced in human breast cancers, which correlates with active aPKC and Stat3. These data identify Par3 as a regulator of signaling pathways relevant to invasive breast cancer.
机译：上皮组织的丧失是癌的标志，但是极性是否能调节肿瘤的生长和转移却知之甚少。为了解决这个问题，我们在小鼠乳腺中通过RNAi与致癌的Notch或Ras61L表达相结合，消除了Par3极性基因。在两个模型中，Par3沉默均可显着降低肿瘤潜伏期，并产生保留上皮标记物表达的浸润性和转移性肿瘤。 Par3消耗与MMP9的诱导，细胞外基质的破坏和侵袭有关，所有这些都由非典型PKC依赖的JAK / Stat3激活介导。重要的是，Par3表达在人乳腺癌中显着降低，这与活性aPKC和Stat3相关。这些数据确定Par3是与浸润性乳腺癌相关的信号通路的调节剂。

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