Expression of 7F7‐antigen, a human adhesion molecule identical to intercellular adhesion molecule‐1 (ICAM‐1) in human carcinomas and their stromal fibroblasts

Vogetseder, Werner; Feichtinger, Hans G.; Schulz, Thomas F.; Schwaeble, Wilhelm; Tabaczewski, Piotr; Mitterer, Manfred; Bouck, G. Benjamin; Marth, Christian; Dapunt, O; Mikuz, Gregor; Dierich, Manfred P.

doi:10.1002/ijc.2910430504

Cited by 76 publications

(43 citation statements)

References 27 publications

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“…Our data suggest the possibility that stromal fibroblasts may indeed facilitate tumour progression, possibly invasion, and metastasis, leading to a higher rate of disease recurrence. Fibroblasts, being both activated by cytokines and at the same time producing cytokines or other soluble factors, were reported to modulate various aspects of tumour progression including proliferation or invasion (Vogetseder et al, 1989;Nakamura et al, 1997), angiogenesis (Orimo et al, 2001), or inhibition of cell death (Olumi et al, 1998). Vimentin expression is reportedly universally found in all types of fibroblasts (Skalli et al, 1989;Sappino et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Quantitative evaluation of vimentin expression in tumour stroma of colorectal cancer

et al. 2007

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Recent studies have identified vimentin, a type III intermediate filament, among genes differentially expressed in tumours with more invasive features, suggesting an association between vimentin and tumour progression. The aim of this study, was to investigate whether vimentin expression in colon cancer tissue is of clinical relevance. We performed immunostaining in 142 colorectal cancer (CRC) samples and quantified the amount of vimentin expression using computer-assisted image analysis. Vimentin expression in the tumour stroma of CRC was associated with shorter survival. Overall survival in the high vimentin expression group was 71.2% compared with 90.4% in the low-expression group (P ¼ 0.002), whereas disease-free survival for the high-expression group was 62.7% compared with 86.7% for the low-expression group (P ¼ 0.001). Furthermore, the prognostic power of vimentin for disease recurrence was maintained in both stage II and III CRC. Multivariate analysis suggested that vimentin was a better prognostic indicator for disease recurrence (risk ratio ¼ 3.5) than the widely used lymph node status (risk ratio ¼ 2.2). Vimentin expression in the tumour stroma may reflect a higher malignant potential of the tumour and may be a useful predictive marker for disease recurrence in CRC patients.

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Section: Discussionmentioning

confidence: 99%

Quantitative evaluation of vimentin expression in tumour stroma of colorectal cancer

et al. 2007

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“…Previous studies which have included ovarian adenocarcinomas scored either 5-30% of cells positive from a single tumour examined (Vogetseder et al, 1989) or found 0/15 primary tumours and 0/9 metastasis positive for ICAM-1 expression (Natali et al, 1990). While the antibody used in these studies was different to that used in this study, the data support our findings that the majority of ovarian tumours express little or no ICAM-1.…”

Section: Discussionmentioning

confidence: 99%

“…There was also frequent LOH at 19p13 (28%) at a similar rate to that reported in previous studies (Amfo et al, 1995;Wang et al, 1999). We found a weak association between this LOH and loss of ICAM-1 expression, suggesting that loss of expression may also be due to LOH in some cases.Expression of ICAM-1 has previously been examined by immunohistochemistry in a variety of human neoplasms including breast cancer, lung cancer, squamous-cell carcinoma, renal cell cancer, pancreatic cancer, gastric cancer, ovarian adenocarcinoma, prostatic cancer, thyroid cancer and malignant melanoma (Johnson et al, 1989;Vogetseder et al, 1989;Natali et al, 1990;Tomita et al, 1990;Koyama et al, 1992; Schwaeble et al, 1993;Ogawa et al, 1998). Previous studies which have included ovarian adenocarcinomas scored either 5-30% of cells positive from a single tumour examined (Vogetseder et al, 1989) or found 0/15 primary tumours and 0/9 metastasis positive for ICAM-1 expression (Natali et al, 1990).…”

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confidence: 99%

Reduced expression of intercellular adhesion molecule-1 in ovarian adenocarcinomas

et al. 2001

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Summary Ovarian adenocarcinomas develop as the result of multiple genetic and epigenetic changes in the precursor ovarian surface epithelial (OSE) cells which result in a malignant phenotype. We investigated changes in gene expression in ovarian adenocarcinoma using a cDNA array containing 588 known human genes. We found that intercellular adhesion molecule-1 (ICAM-1) was expressed at lower levels in the ovarian tumour cell lines OAW42, PEO1 and JAM than in the immortalised human ovarian surface epithelial cell line HOSE 17.1. Further investigation revealed ICAM-1 was expressed in the surface epithelium of normal ovaries and both mRNA and protein expression levels were reduced in the majority of ovarian adenocarcinoma cell lines and primary tumours. ICAM-1 expression was increased in 8/8 cell lines treated with the de novo methyltransferase inhibitor 5-aza-2′-deoxycytidine, indicating that methylation of CpG islands may play a role in the down-regulation of its expression in primary tumours. There was a significant association between patients whose tumours expressed ICAM-1 and survival (P = 0. 1351-1358© 2001 Cancer Research Campaign doi: 10.1054/ bjoc.2001.2075, available online at http://www.idealibrary.com on http://www.bjcancer.com 1987), SKOV3 (Fogh and Trempe, 1975), COLO316 (Woods et al, 1979), CAOV3 (Wong et al, 1999), OVCAR-3 (Hamilton et al, 1983) and 27/87 (derived by T Hurst) -were all maintained in RPMI 1640 with 10% FCS. Cells were harvested for RNA isolation at about 80% confluence. The cell lines OAW 42, PEO1, PEO14, JAM, SKOV3 and COLO316 were derived from serous tumours, and 27/87 was from an endometrioid tumour. The histological types of the tumours from which the cell lines HEY, CAOV3 and OVCAR3 were derived are unknown.Primary cultures of human ovarian surface epithelial (OSE) cells were prepared according to the method of Kruk et al (1990). Epithelial cells were obtained by scraping contaminating stromal cells away from proliferating epithelial sheets and were cultured in 1:1 MCDB105: Medium 199 with Earles' salts, supplemented with 20 ng ml -1 epidermal growth factor, 400 ng ml -1 hydrocortisone and 15% fetal calf serum. Their distinctive cellular morphology was used to confirm that the cultures were epithelial cells. In one case, RNA was extracted directly from the peeled epithelial cells without culturing.Ovarian adenocarcinomas were obtained from 44 patients undergoing surgery. There were 35 serous, 6 endometrioid, one mucinous and 2 clear-cell tumours. There were 43 malignant tumours and the other was of low malignant potential (LMP). All patients were staged at laparotomy, in accordance with the recommendations of the International Federation of Gynaecology and Obstetrics (FIGO). Of the malignant tumours, one was FIGO stage 1, 4 stage 2, 33 stage 3 and 5 stage 4. There were two grade 1-2, 11 grade 2, 10 grade 2/3, 17 grade 3, one grade 3-4, and 2 that were not graded. Clinicopathological data for these tumours are summarised in Table 2. Constitutional DNA was available in all ca...

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“…Altogether, these results provide evidence of an important role for Ets-related transcription factors, and more particularly the PEA3 group members, in tumor cell invasion. Strong ICAM-1 expression is found in solid tumors such as melanomas and renal carcinomas and in a lesser extent in gastric, breast and colorectal carcinomas (Vogetseder et al, 1989;Natali et al, 1990;Johnson, 1991). As far as melanoma are concerned, de novo ICAM-1 expression correlates with increased risk of metastasis (Johnson et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

The transcription of the intercellular adhesion molecule-1 is regulated by Ets transcription factors

Launoit

Audette²,

Pelczar

et al. 1998

Oncogene

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The Ets family of transcription factors comprises several members which are involved to regulate gene transcription. Although several consensus binding sites for Ets proteins can be found in a wide series of promoter, only a limited number of them are indeed activated by these transcription factors. The human intercellular adhesion molecule-1 (ICAM-1) plays a crucial role in immune responses by enabling the binding of eector cells to various target cell types. ICAM-1 is constitutively expressed at dierent levels in the absence of stimuli in dierent cell types, and its expression is upregulated by several proin¯ammatory cytokines. We have here examined the transcriptional regulation of human ICAM-1 expression by Ets proteins, and more particularly by ERM, a member of this family of transcription factors. Transient transfection assays revealed that Ets-2 and ERM signi®cantly activate the transcription of ICAM-1 promoter, whereas the less-related Ets family member, Spi-1/Pu.1, failed to do so. Transfection of a series of ICAM-1 promoter deletion mutants together with ERM expression plasmids have shown that an Ets responsive element is located within the ®rst 176 bp upstream from the translational start site. Electrophoretic mobility shift assays and DNase I footprinting analysis have enabled us to identify two Ets binding sites at positions 7158 and 7138 from the ATG, respectively. Site directed mutagenesis of these elements has shown that the distal site is the major element required for the ERM-mediated activation of the ICAM-1 promoter. We can thus conclude that expression of ICAM-1 can be regulated by Ets transcription factors.

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Expression of 7F7‐antigen, a human adhesion molecule identical to intercellular adhesion molecule‐1 (ICAM‐1) in human carcinomas and their stromal fibroblasts

Cited by 76 publications

References 27 publications

Quantitative evaluation of vimentin expression in tumour stroma of colorectal cancer

Quantitative evaluation of vimentin expression in tumour stroma of colorectal cancer

Reduced expression of intercellular adhesion molecule-1 in ovarian adenocarcinomas

The transcription of the intercellular adhesion molecule-1 is regulated by Ets transcription factors

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