ERBB-2 overexpression confers PI 3' kinase-dependent invasion capacity on human mammary epithelial cells.
ERBB-2 overexpression confers PI 3' kinase-dependent invasion capacity on human mammary epithelial cells.
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ERBB-2 过表达赋予人乳腺上皮细胞 PI 3' 激酶依赖性侵袭能力。
DOI：
10.1054/bjoc.1999.0979
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发表时间：
2000-02
影响因子：
8.8
通讯作者：
Ethier SP
中科院分区：
文献类型：
--
作者：
Ignatoski KM;Maehama T;Markwart SM;Dixon JE;Livant DL;Ethier SP
ERBB-2 在人类乳腺癌中的扩增和过度表达被认为在疾病的进展中发挥着重要作用；然而，其在与人类乳腺癌相关的表型改变的病因学中的确切作用尚不清楚。我们之前已经证明，外源性过度表达 ERBB-2 赋予人乳腺上皮细胞生长因子独立性。在这项研究中，我们发现 ERBB-2 过度表达还会导致细胞获得人类乳腺癌细胞所表现出的其他特征，例如不依赖贴壁的生长和侵袭能力。 ERBB-2 诱导的侵袭依赖于纤连蛋白，并与细胞表面 α4 整合素的下调相关。此外，ERBB-2 与这些细胞中的粘着斑激酶 (FAK) 发生共免疫沉淀。我们还通过使用外源表达的 PTEN 和 PI3'-激酶抑制剂 LY294002 治疗表明，ERBB-2 诱导的侵袭依赖于 PI3'-激酶途径；然而，PTEN 不会使这些细胞中的 FAK 去磷酸化。 © 2000 年癌症研究运动
Amplification and overexpression of ERBB-2 in human breast cancer is thought to play a significant role in the progression of the disease; however, its precise role in the aetiology of altered phenotypes associated with human breast cancer is unknown. We have previously shown that exogenous overexpression of ERBB-2 conferred growth factor independence on human mammary epithelial cells. In this study, we show that ERBB-2 overexpression also causes the cells to acquire other characteristics exhibited by human breast cancer cells, such as anchorage-independent growth and invasion capabilities. ERBB-2-induced invasion is dependent on fibronectin and correlates with the down-regulation of cell surface α4 integrin. In addition ERBB-2 co-immunoprecipitates with focal adhesion kinase (FAK) in these cells. We have also shown, by use of exogenously expressed PTEN and by treatment with the PI3′-kinase inhibitor LY294002, that ERBB-2-induced invasion is dependent on the PI3′-kinase pathway; however, PTEN does not dephosphorylate FAK in these cells. © 2000 Cancer Research Campaign
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