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Simultaneous E-cadherin and PLEKHA7 expression negatively affects E-cadherin/EGFR mediated ovarian cancer cell growth

机译:E-钙粘蛋白和PLEKHA7同时表达对E-钙粘蛋白/ EGFR介导的卵巢癌细胞生长产生负面影响

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摘要

BackgroundThe disruption of E-cadherin-mediated adhesion is considered an important driver of tumor progression. Nevertheless, numerous studies have demonstrated that E-cadherin promotes growth- or invasion-related signaling, contrary to the prevailing notion. During tumor progression, epithelial ovarian cancer (EOC) maintains E-cadherin expression and can positively affect EOC cell growth by contributing to PI3K/AKT activation. In polarized epithelia PLEKHA7, a regulator of the zonula adherens integrity, impinges E-cadherin functionality, but its role in EOCs has been never studied.
机译:背景E-钙粘蛋白介导的粘附的破坏被认为是肿瘤进展的重要驱动力。然而,许多研究表明,E-钙粘着蛋白能促进与生长或入侵相关的信号传导,这与流行的观念相反。在肿瘤进展过程中,上皮性卵巢癌(EOC)维持E-钙黏着蛋白表达,并通过促进PI3K / AKT激活而积极影响EOC细胞的生长。在极化的上皮PLEKHA7中,小带的调节子粘附完整性,影响E-钙粘蛋白功能,但从未研究过其在EOC中的作用。

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