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首页> 外文期刊>Cancer Cell >Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis.
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Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis.

机译：E-cadherin和p53的小鼠体细胞失活可通过诱导失常抗药性和血管生成而导致转移性小叶型乳腺癌。

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摘要

Metastatic disease is the primary cause of death in breast cancer, the most common malignancy in Western women. Loss of E-cadherin is associated with tumor metastasis, as well as with invasive lobular carcinoma (ILC), which accounts for 10%-15% of all breast cancers. To study the role of E-cadherin in breast oncogenesis, we have introduced conditional E-cadherin mutations into a mouse tumor model based on epithelium-specific knockout of p53. Combined loss of E-cadherin and p53 resulted in accelerated development of invasive and metastatic mammary carcinomas, which show strong resemblance to human ILC. Moreover, loss of E-cadherin induced anoikis resistance and facilitated angiogenesis, thus promoting metastatic disease. Our results suggest that loss of E-cadherin contributes to both mammary tumor initiation and metastasis.
机译：转移性疾病是乳腺癌的主要死因，而乳腺癌是西方女性最常见的恶性肿瘤。 E-钙粘蛋白的丢失与肿瘤转移以及浸润性小叶癌（ILC）有关，后者占所有乳腺癌的10％-15％。为了研究E-钙粘蛋白在乳腺肿瘤发生中的作用，我们将基于条件的E-钙粘蛋白突变引入基于p53上皮特异性敲除的小鼠肿瘤模型中。 E-钙黏着蛋白和p53的共同丧失导致浸润性和转移性乳腺癌的发展加快，这与人ILC非常相似。此外，E-钙粘着蛋白的丧失引起神经阻逆性并促进血管生成，从而促进转移性疾病。我们的结果表明，E-钙粘着蛋白的丢失有助于乳腺肿瘤的发生和转移。

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