Coexpression of keratin- and vimentin-type intermediate filaments in human metastatic carcinoma cells.

Ramaekers, F.C.S.; Haag, D.; Kant, A.; Moesker, O.; Jap, P. H. K.; Vooijs, G. P.

doi:10.1073/pnas.80.9.2618

Cited by 250 publications

(86 citation statements)

References 26 publications

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“…When CK5/6 has been tested on histological material from lung tumors, reactivity has been found in a small proportion of lung adenocarcinomas (14,15). In the present study, the frequency of CK5/6 positivity was considerably higher than in reports based on the results obtained with histological sections.…”

Section: Discussioncontrasting

confidence: 56%

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The reactivity to CK5/6 antibody in tumor cells from non-small cell lung cancers shed into pleural effusions predicts survival

Dejmek

2006

Oncol Rep

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Abstract. Lung cancer, especially adenocarcinoma and large cell carcinoma, tends to spread to the pleural cavities. Once an effusion develops, the prognosis is generally dismal.Immunocytochemistry is frequently applied to effusions for diagnostic purposes, but the prognostic value of markers in malignant effusions have thus far attracted less attention. Dakopatts CK 5/6 antibody was applied to ethanol-fixed fresh cytospin preparations from malignant pleural effusions originating from 18 patients (11 men and 7 women) with a previously or later verified non-small cell lung carcinoma (NSCLC). In three cases, CK5/6 reactivity was found in part of the malignant population, whereas 10 cases showed reactivity in most tumor cells. The lack of reactivity in malignant cells was only seen in five effusions. Females showed significantly lower reactivity rates, with all negative effusions coming from female patients, whereas 9/10 effusions with reactivity in most malignant cells originated from males. CK5/6 reactivity was significantly correlated to survival, with a median survival time of 18 days for patients with CK5/6-negative tumors, and 212 days for those with positive tumors. The strong relationship between CK5/6 reactivity and survival, and the observed gender difference, warrants larger studies aimed at the clinical utility of CK5/6 as a prognostic marker in metastatic NSCLC, the possible functional role of CK5/6 in cell adhesion in advanced NSCLC and its possible hormonal control.

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Section: Discussioncontrasting

confidence: 56%

“…The biological reasons for discrepancies between immunoreactivity in primary tumors and metastatic cells in effusions include the fact that the immunophenotype may change during tumor progression, and cells that are shed into effusions may reveal another immunophenotype than cells fixed in solid tissue (15)(16)(17)(18).…”

Section: Discussionmentioning

confidence: 99%

The reactivity to CK5/6 antibody in tumor cells from non-small cell lung cancers shed into pleural effusions predicts survival

Dejmek

2006

Oncol Rep

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“…However, one marker of both myoepithelial and mesenchymal cells is retained, that of vimentin (Warburton et al, 1989). The changed subcellular location of milk fat globule membrane antigen and the receptor for peanut lectin from a predominantly membranous to a more cytoplasmic distribution (Sloane and Ormerod, 1981) and the expression of vimentin (Ramaekers et al, 1983) are features which are also observed in malignant epithelial cells of some human breast carcinomas (Rudland, 1993). Although staining for laminin is largely lost in these malignant cells there is an apparent increase in the number of laminin-staining vessels particularly at the leading edges of tumours/metastases.…”

Section: Discussionmentioning

confidence: 99%

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

et al. 1998

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The rodent S100-related calcium-binding protein, S100A4 induces metastasis in non-metastatic rat and mouse benign mammary cells and co-operates with benign-tumour-inducing changes in two transgenic mouse models, to yield metastatic mammary tumours. Cotransfection of the human gene for S100A4 with pSV2neo into the benign rat mammary cell line, Rama 37, yielded cells which expressed a low level of the endogenous S100A4 mRNA, and either high or undetectable levels of human S100A4 mRNA. The cells which expressed a high level of human S100A4 mRNA induced metastasis in the benign rat mammary cell line Rama 37 in an in vivo assay, whereas the cells which expressed an undetectable level of human S100A4 did not induce any detectable metastases. The primary tumours arising from the S100A4-expressing cells contained high levels of immunocytochemically-detected S100A4 and this high level of S100A4 and the metastatic potential were maintained when cells from a metastasis were re-injected into syngeneic rats. The results show that the human S100A4 possesses metastasis-inducing capabilities.

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“…However, numerous data have now demonstrated that vimentin can also be expressed in epithelial cells when they become involved in physiological or pathological processes requiring epithelial cell migration. Vimentin has indeed been described in migratory epithelial cells involved in embryonic and organogenesis processes, in placentation, wound healing and tumor invasion (Ramaekers et al, 1983;Guarino, 1995;Gilles and Thompson, 1996;Gilles et al, 1999Gilles et al, , 2003. Also, vimentin-specific antisense cDNA or oligonucleotide transfection in vimentin-expressing cell lines was shown to reduce their in vitro invasiveness or migration, strongly emphasizing a functional contribution of vimentin to epithelial cell invasion/migration (Hendrix et al, 1997;Gilles et al, 1999;Singh et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Regulation of vimentin by SIP1 in human epithelial breast tumor cells

et al. 2006

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The expression of Smad interacting protein-1 (SIP1; ZEB2) and the de novo expression of vimentin are frequently involved in epithelial-to-mesenchynial transitions (EMTs) under both normal and pathological conditions. In the present study, we investigated the potential role of SIP1 in the regulation of vimentin during the EMT associated with breast tumor cell migration and invasion. Examining several breast tumor cell Unes displaying various degrees of invasiveness, we found SIP1 and vimentin expression only in invasive cell Unes. Also, using a model of cell migration with human mammary MCF10A cells, we showed that SIP1 is induced specifically in vimentin-positive migratory cells. Furthermore, transfection of SIP1 cDNA in MCF10A cells increased their vimentin expression both at the mRNA and protein levels and enhanced their migratory abilities in Boyden Chamber assays. Inversely, inhibition of SIP1 expression by RNAi strategies in BT-549 cells and MCF10A cells decreased vimentin expression. We also showed that SIP1 transfection did not activate the TOP-FLASH reporter system, suggesting that the β-catenin/ TCF pathway is not impUcated in the regulation of vimentin by SIP1. Our results therefore impUcate SIP1 in the regulation of vimentin observed in the EMT associated with breast tumor cell migration, a pathway that may contribute to the metastatic progression of breast cancer.

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Coexpression of keratin- and vimentin-type intermediate filaments in human metastatic carcinoma cells.

Cited by 250 publications

References 26 publications

The reactivity to CK5/6 antibody in tumor cells from non-small cell lung cancers shed into pleural effusions predicts survival

The reactivity to CK5/6 antibody in tumor cells from non-small cell lung cancers shed into pleural effusions predicts survival

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

Regulation of vimentin by SIP1 in human epithelial breast tumor cells

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