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EpCAM-claudin-tetraspanin-modulated ovarian cancer progression and drug resistance.
Cell Adhesion & Migration ( IF 3.2 ) Pub Date : 2020-02-24 , DOI: 10.1080/19336918.2020.1732761
Zehra Tavsan 1, 2 , Hülya Ayar Kayalı 2, 3, 4
Affiliation  

ABSTRACT

Alterations of cell adhesion are involved in cancer progression, but the mechanisms underlying the progression and cell adhesion have remained poorly understood. Focusing on the complex between EpCAM, claudins and tetraspanins, we described a sequence of events by which of the molecules associate each other in ovarian cancer. The interactions between molecules were evaluated by immunoprecipitations and then immunoblotting. To identify the effects of complex formation on the ovarian cancer progression, the different types of ovarian cancer cell lines were compared. In this study, we report the identification of the EpCAM-claudin-4 or −7-CD82 complex in the ovarian cancer progression and metastasis in vitro. Additionally, we demonstrated palmitoylation and intra- or extra-cellular regions are critically required for the complex formation. These results represent the first direct evidence for the link between the dynamism of cell adhesion molecules and ovarian cancer progression.



中文翻译:

EpCAM-claudin-tetraspanin调节的卵巢癌进展和耐药性。

摘要

细胞粘附的改变与癌症的进展有关,但对进展和细胞粘附的机制仍知之甚少。着眼于EpCAM,claudins和tetraspanins之间的复合物,我们描述了一系列事件,通过这些事件分子在卵巢癌中彼此缔合。分子之间的相互作用通过免疫沉淀然后进行免疫印迹来评估。为了确定复合物形成对卵巢癌进展的影响,比较了不同类型的卵巢癌细胞系。在这项研究中,我们报告了在体外卵巢癌进展和转移中鉴定EpCAM-claudin-4或-7-CD82复合物。此外,我们证明了棕榈酰化和细胞内或细胞外区域是形成复合物的关键条件。

更新日期:2020-02-24
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