Epithelial and stromal syndecan-1 expression as predictor of outcome in patients with gastric cancer

Wiksten, Jan-Patrik; Lundin, Johan; Nordling, Stig; Lundin, Mikael; Kokkola, Arto; Boguslawski, Kristina von; Haglund, Caj

doi:10.1002/1097-0215(20010120)95:1<1::aid-ijc1000>3.0.co;2-5

Cited by 93 publications

(91 citation statements)

References 20 publications

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“…The expression of syndecan-1 inversely correlates with metastasis and positively correlates with a more favorable prognosis in several epithelial cancers (Inki and Jalkanen, 1996;Wiksten et al, 2001). However, it is noteworthy that Eph receptors and ephrin B ligands are expressed in several cancer cell lines and tumor tissues (Tang et al, 1999) and that the expression of ephrin B2 is associated with invasion occurrence in endometrial cancer (Takai et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Syntenin is overexpressed and promotes cell migration in metastatic human breast and gastric cancer cell lines

et al. 2002

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Two human breast cancer cell lines of di ering invasive and metastatic potential, MDA-MB-435 and MCF7, were examined using subtractive suppression hybridization in a search for any genes associated with metastasis. Of the 17 cDNAs identi®ed as being di erentially expressed genes, it was determined that syntenin was overexpressed in metastatic MDA-MB-435 cells. Expression analysis showed that the expression level of syntenin was well correlated with invasive and metastatic potential in various human breast and gastric cancer cell lines. Moreover, gastric tumor tissues exhibited a much higher syntenin mRNA expression than their normal counterparts. Syntenin-transfected MCF7 cells migrated more actively, and showed an increased invasion rate relative to vector-transfectants or parental MCF7 in vitro, without evidencing any e ect on the adhesion to ®bronectin, type I collagen and laminin. Similarly, the forced expression of syntenin to human gastric cancer cell line Az521 increased its migratory and invasive potential in vitro. Syntenin-expressing MCF7 cells were associated with the appearance of numerous cell surface extensions and with pseudopodia formation on collagen I, suggesting that syntenin may be involved in the signaling cascade to actin-reorganization. Mutation study suggested that PDZ2 domain of syntenin could be an essential role in its stimulatory e ect on the cell migration. This is the ®rst demonstration that syntenin, a PDZ motif-containing protein, can be overexpressed during the metastatic progression of human breast and gastric cancer cells and that it can function as a metastasis-inducing gene.

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Section: Discussionmentioning

confidence: 99%

Syntenin is overexpressed and promotes cell migration in metastatic human breast and gastric cancer cell lines

et al. 2002

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“…In general, syndecans are known to suppress tumor formation and their expressions are downregulated in transformed/cancer cells (Bernfield et al, 1992;Leppa et al, 1992;Inki andJalkanen, 1996, Jayson et al, 1999;Wiksten et al, 2001). However, this study clearly shows that syndecan-2 expression is important for tumor formation in colon carcinoma cells, since (1) expression of syndecan-2 was increased compared to syndecan-1 and -4 (Figure 3), and (2) decreased syndecan-2 expression by either TSA treatment or antisense syndecan-2 cDNA induced the morphological change and reduced tumorigenic activity (Figure 4).…”

Section: Tsa-induced Morphological Changes Y Kim Et Almentioning

confidence: 99%

Decreased syndecan-2 expression correlates with trichostatin-A induced-morphological changes and reduced tumorigenic activity in colon carcinoma cells

et al. 2003

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The inhibition of histone deacetylase activity is known to induce morphological changes of transformed cells. In this study, we investigated the effect of the specific HDAC inhibitor, trichostatin A (TSA), on colon carcinoma cell lines. Treatment of human colorectal carcinoma cells, KM1214 and KM12SM, with TSA induced distinct morphological changes. Both cell lines, which normally piled up in layers without clear boundary, became more flattened, and formed monolayers with evident boundaries between cells, with concomitant increased actin filament organization. Cell-cell interaction was not affected much, based on expression level, membrane localization, and interaction of E-cadherin with b-catenin. In contrast, syndecan-2 expression was dramatically reduced and it was correlated with the morphological changes of colon carcinoma cells. Consistently, downregulation of syndecan-2 expression by antisense cDNA clearly mimicked the morphological changes in KM12SM and reduced anchorage-independent growth of colon cancer cells. All these results indicate that reduced syndecan-2 expression correlates with TSA-induced morphological changes and reduced tumorigenic activity in colon carcinoma cells.

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“…Expression of syndecan-1 is inhibited by malignant transformation of human keratinocytes (6). Moreover, syndecan-1 expression is decreased in a variety of cancer tissues (7)(8)(9)(10)(11)(12). Similarly, syndecan-4, which is mainly involved in cytoskeletal and membrane reorganization to form stress fibers and focal adhesions at the later stage of primary fibroblast spreading (13), inhibits cell migration and tumor activity (14 -16).…”

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confidence: 99%

Syndecan-2 Mediates Adhesion and Proliferation of Colon Carcinoma Cells

Park¹,

Kim²,

Lim³

et al. 2002

Journal of Biological Chemistry

151

130

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Syndecan-2 is a transmembrane heparan sulfate proteoglycan whose function at the cell surface is unclear. In this study, we examined the function of syndecan-2 in colon cancer cell lines. In several colon cancer cell lines, syndecan-2 was highly expressed compared with normal cell lines. In contrast, syndecan-1 and -4 were decreased. Cell biological studies using the extracellular domain of recombinant syndecan-2 (2E) or spreading assay with syndecan-2 antibody-coated plates showed that syndecan-2 mediated adhesion and cytoskeletal organization of colon cancer cells. This interaction was critical for the proliferation of colon carcinoma cells. Blocking with 2E or antisense syndecan-2 cDNA induced G 0 /G 1 cell cycle arrest with concomitantly increased expression of p21, p27, and p53. Furthermore, blocking of syndecan-2 through antisense syndecan-2 cDNA significantly reduced tumorigenic activity in colon carcinoma cells. Therefore, increased syndecan-2 expression appears to be a critical for colon carcinoma cell behavior, and syndecan-2 regulates tumorigenic activity through regulation of adhesion and proliferation in colon carcinoma cells.

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Epithelial and stromal syndecan-1 expression as predictor of outcome in patients with gastric cancer

Cited by 93 publications

References 20 publications

Syntenin is overexpressed and promotes cell migration in metastatic human breast and gastric cancer cell lines

Syntenin is overexpressed and promotes cell migration in metastatic human breast and gastric cancer cell lines

Decreased syndecan-2 expression correlates with trichostatin-A induced-morphological changes and reduced tumorigenic activity in colon carcinoma cells

Syndecan-2 Mediates Adhesion and Proliferation of Colon Carcinoma Cells

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