P-Cadherin Is Up-Regulated by the Antiestrogen ICI 182,780 and Promotes Invasion of Human Breast Cancer Cells

Paredes, Joana; Stove, Christophe; Stove, Veronique; Milanezi, Fernanda; Derycke, Lara; Mareel, Marcus; Bracke, Marc; Schmitt, Fernando

doi:10.1158/0008-5472.can-04-0795

Cited by 70 publications

(90 citation statements)

References 49 publications

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“…Previous studies have shown that P-cadherin expression in breast carcinomas is able to identify a subgroup of lesions with a more aggressive behaviour and poor patient survival (Peralta Soler et al, 1999;Gamallo et al, 2001;Paredes et al, 2002Paredes et al, , 2004Paredes et al, , 2005Paredes et al, , 2008. Similar associations between P-cadherin expression and poor prognosis are described in other cancer models, namely endometrial, cervical, gastric and pancreatic carcinomas (Stefansson et al, 2004;Longatto Filho et al, 2005;Taniuchi et al, 2005).…”

Section: Discussionmentioning

confidence: 67%

“…Our group has previously shown in vitro that, using HEK 293 T cells as a model system, P-cadherin has a pro-invasive activity, through its juxtamembrane domain (Paredes et al, 2004). In contrast, in highly invasive melanoma cell lines, P-cadherin overexpression is able to promote the formation of cell-cell contacts and counteract invasion (Van Marck et al, 2005), showing that it may function either as an invasion promoter or as an invasion suppressor depending on tissue specificity.…”

Section: Discussionmentioning

confidence: 99%

“…All the media contained 10% heat-inactivated fetal bovine serum (Greiner bio-one, Wemmel, Belgium), 100 IU/ml penicillin and 100 mg/ml streptomycin. MCF-7/AZ cell line was retrovirally stable transduced to encode P-cadherin (MCF-7/AZ.Pcad cell line), as described earlier (Paredes et al, 2004). MCF-7/ AZ.Mock cell line, encoding only EGFP, was used as a control.…”

Section: Cell Culture and Transfectionmentioning

confidence: 99%

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Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

et al. 2009

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Cell-cell adhesion is an elementary process in normal epithelial cellular architecture. Several studies have shown the role mediated by cadherins in this process, besides their role in the maintenance of cell polarity, differentiation and cell growth. However, during tumour progression, these molecules are frequently altered. In breast cancer, tumours that overexpress P-cadherin usually present a high histological grade, show decreased cell polarity and are associated with worse patient survival. However, little is known about how this protein dictates the very aggressive behaviour of these tumours. To achieve this goal, we set up two breast cancer cell models, where P-cadherin expression was differently modulated and analysed in terms of cell invasion, motility and migration. We show that P-cadherin overexpression, in breast cancer cells with wild-type E-cadherin, promotes cell invasion, motility and migration. Moreover, we found that the overexpression of P-cadherin induces the secretion of matrix metalloproteases, specifically MMP-1 and MMP-2, which then lead to P-cadherin ectodomain cleavage. Further, we showed that soluble P-cadherin fragment is able to induce in vitro invasion of breast cancer cells. Overall, our results contribute to elucidate the mechanism underlying the invasive behaviour of P-cadherin expressing breast tumours.

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Section: Discussionmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Section: Cell Culture and Transfectionmentioning

confidence: 99%

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Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

et al. 2009

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“…194), and cell adhesion molecules (e.g., E-cadherin and P-cadherin; refs. [195][196][197][198] have been studied as possible breast tumor markers. In this context, osteopontin also represents an interesting alternative as a breast cancer marker.…”

Section: Breast Cancer Biomarkersmentioning

confidence: 99%

The Role of Osteopontin in Tumor Progression and Metastasis in Breast Cancer

Rodrigues

Teixeira

Schmitt

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

206

144

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The use of cancer biomarkers to anticipate the outlines of disease has been an emerging issue, especially as cancer treatment has made such positive steps in the last few years. Progress in the development of consistent malignancy markers is imminent because advances in genomics and bioinformatics have allowed the examination of immense amounts of data. Osteopontin is a phosphorylated glycoprotein secreted by activated macrophages, leukocytes, and activated T lymphocytes, and is present in extracellular fluids, at sites of inflammation, and in the extracellular matrix of mineralized tissues. Several physiologic roles have been attributed to osteopontin, i.e., in inflammation and immune function, in mineralized tissues, in vascular tissue, and in kidney. Osteopontin interacts with a variety of cell surface receptors, including several integrins and CD44. Binding of osteopontin to these cell surface receptors stimulates cell adhesion, migration, and specific signaling functions. Overexpression of osteopontin has been found in a variety of cancers, including breast cancer, lung cancer, colorectal cancer, stomach cancer, ovarian cancer, and melanoma. Moreover, osteopontin is present in elevated levels in the blood and plasma of some patients with metastatic cancers. Therefore, suppression of the action of osteopontin may confer significant therapeutic activity, and several strategies for bringing about this suppression have been identified. This review looks at the recent advances in understanding the possible mechanisms by which osteopontin may contribute functionally to malignancy, particularly in breast cancer. Furthermore, the measurement of osteopontin in the blood or tumors of patients with cancer, as a way of providing valuable prognostic information, will be discussed based on emerging clinical data. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1087 -97)

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“…Hormonal regulation of cadherins levels has been shown for the estrogen receptor, which modulates Snail repression of E-cadherin levels during invasive growth of breast cancers (reviewed in Fearon, 2003). In addition, antiestrogens result in upregulation of P-cadherin occurs in proliferative, invasive breast cancer cells (Paredes et al, 2004).…”

Section: Ecr Is Required For Fc Migration and Differentiationmentioning

confidence: 99%

Ras signaling modulates activity of the ecdysone receptor EcR during cell migration in the drosophila ovary

Hackney

Pucci

Naes

et al. 2007

Developmental Dynamics

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Ecdysone Receptor (EcR) mediates effects of the hormone ecdysone during larval molts, pupal metamorphosis, and adult female oogenesis. In the ovary, egg chamber formation requires interactions between the somatic follicle cell (FC) epithelium and the germ line nurse cell/oocyte cyst. Previous work has shown EcR is required in the germ line for egg chamber maturation, and here we examine EcR requirements in the FC at late stages of oogenesis. EcR protein is ubiquitous in the FC but its activity is restricted, visualized by activity of the "ligand sensor" hs-GAL4-EcR ligand binding domain fusion and

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P-Cadherin Is Up-Regulated by the Antiestrogen ICI 182,780 and Promotes Invasion of Human Breast Cancer Cells

Cited by 70 publications

References 49 publications

Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

The Role of Osteopontin in Tumor Progression and Metastasis in Breast Cancer

Ras signaling modulates activity of the ecdysone receptor EcR during cell migration in the drosophila ovary

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