Original contributionExpression of E-cadherin and N-cadherin in surface epithelial-stromal tumors of the ovary distinguishes mucinous from serous and endometrioid tumors☆
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EMT, MET, Plasticity, and Tumor Metastasis
2020, Trends in Cell BiologyCitation Excerpt :Under these experimental conditions, Ecad expression is maintained, although EMT-TF expression is largely unperturbed [48]. The ovarian surface epithelium, from which most ovarian cancers derive, is normally Ecad- [49], but it shows a remarkable upregulation of Ecad during ovarian cancer progression [49–52]. This acquisition of Ecad at the primary tumor site in ovarian cancers is not reversed during omental metastasis [53], and ovarian cancer cells in pleural and peritoneal effusions show Ecadhigh levels [54].
Scaffold-free parathyroid tissue engineering using tonsil-derived mesenchymal stem cells
2016, Acta BiomaterialiaCitation Excerpt :It was previously reported that hESC express E-cadherin, which is involved in increasing spheroidal formation through inhibition of Wnt signaling [34]. E-cadherin is known to be of epithelial origin, whereas N-cadherin is of mesodermal origin [35]. In this context, TMSC are likely to be mixed cells originating from both endoderm and mesoderm [30,36].
E-cadherin's dark side: Possible role in tumor progression
2012, Biochimica et Biophysica Acta - Reviews on CancerCitation Excerpt :SAHA treatment was also associated with a redistribution of E-cadherin from cell surface to cytoplasm, thus interfering with homotypic cell aggregation despite preserving total E-cadherin levels. Among epithelial cancers, ovarian carcinoma is a prominent exception to the EMT rule: E-cadherin is expressed in the vast majority of ovarian carcinomas, irrespective of histologic type and degree of differentiation, but is low to absent in normal ovarian tissues [64–67] (Fig. 2a). High levels of E-cadherin are ubiquitous in primary ovarian carcinomas, and are also maintained when ovarian carcinoma metastasizes to the peritoneum and omentum [68], a hallmark of this tumor.
E-cadherin nuclear staining is useful for the diagnosis of ovarian adult granulosa cell tumor
2012, Human PathologyCitation Excerpt :The nuclear expression of E-cadherin has never been described in the literature, although varying degrees of membranous staining have been observed [17-28]. In the literature, a total of 145 cases of serous [19,25,27-29] and 10 cases of endometrioid [27,29] adenocarcinomas were investigated by using an anti–E-cadherin antibody recognizing the cytoplasmic domain (clone 36 supplied by BD Biosciences), and the results were consistent with ours (E-cadherin nuclear staining was not observed). In our study, we selected sections of serous adenocarcinoma that were composed of solid proliferation, mimicking the diffuse pattern of AGCT.
S1P and LPA have an attachment-dependent regulatory effect on invasion of epithelial ovarian cancer cells
2007, Gynecologic OncologyCitation Excerpt :The level of N-cadherin in the membrane is probably modulated through translocation to the cytoplasm, which is much richer in N-cad such that its concentration changes little when the membrane portion is added. Previous reports associated N-cadherin expression with enhanced cell migration and motility of breast, prostate and squamous carcinomas [37–39]; however, there are also reports of down-regulation of N-cadherin in metastasic and advanced stage osteosarcoma [40], astrocytic tumors [41], ovarian cancer [42–44] and stimulation of arterial smooth muscle cell migration as result of N-cadherin down-regulation [45]. Overexpression of N-cadherin inhibited in vivo metastasis of osteosarcoma in mice [46].
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Supported in part by NIH 1R41 CA 73093 to (A.P.S.).