Role of tissue stroma in cancer cell invasion

Wever, Olivier De; Mareel, Marcus

doi:10.1002/path.1398

Cited by 925 publications

(860 citation statements)

References 242 publications

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“…27 On the other hand, ECM deposition seems to provide proinvasive signals. 28,29 Tenascin, which is upregulated in the invasion front in our model, provides proinvasive signals to colon cancer cells. 30 Finally, the differentially upregulated ECM molecules fibronectin and collagen IV have proangiogenic properties.…”

Section: Discussionmentioning

confidence: 86%

“…31 The most likely candidate cells responsible for ECM production are HSCs, which are transformed into myofibroblasts upon activation by profibrogenic signals. 28,29 Their role in hepatic fibrosis has been described to a significant extent and HSCs have been described to be the major source of ECM in the liver. 32,33 We therefore examined whether the patterns of gene expression on the single gene level would confirm an enrichment or activation of HSCs in the invasion front.…”

Section: Discussionmentioning

confidence: 99%

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Global analysis of host tissue gene expression in the invasive front of colorectal liver metastases

Bandapalli

Geheeb

Kobelt

et al. 2005

Intl Journal of Cancer

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Host cell reactions are a crucial determinant for tumor invasion. We analyzed on a genomewide scale gene expression differences between microdissected tissues taken from unaffected liver tissue of a human colorectal tumor (LS174) growing in the livers of nude mice and tissue from the host part of the invasive front. Due to the low degree of interspecies cross‐hybridization of 15% as determined on Affymetrix microarrays, our xenograft model allowed for the distinction of genes of murine versus human origin even if the respective tissues could not be isolated separately. Using the gene ontology (GO) classification, we were able to determine patterns of up‐ and downregulated genes in the liver part of the invasive front. We observed a pronounced overrepresentation, e.g., of the GO terms “extracellular matrix,” “cell communication,” “response to biotic stimulus,” “structural molecule activity” and “cell growth,” indicating a very pronounced host cell response to tumor invasion. On the single gene level, hepatic stellate cell (HSC) activation markers were overrepresented in the liver part of the invasion front. Immunohistochemistry and qPCR confirmed an activation of HSC as well as an increased number of HSC in the invasive front as compared to the noninvaded liver tissue. In summary, our data demonstrate the feasibility of an interspecies differential gene expression approach on a genomewide scale. © 2005 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Global analysis of host tissue gene expression in the invasive front of colorectal liver metastases

Bandapalli

Geheeb

Kobelt

et al. 2005

Intl Journal of Cancer

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“…This effect may be mediated directly through cell-cell contacts or through diffusible molecules which are produced and secreted by myofibroblasts. 21,22 They synthesize collagen I and III, fibronectin, versican, vascular endothelial growth factors (VEGFs) (especially type VEGF-D), SDF 1 and tenascin and also express proteases, fibroblasts activation protein and matrix metalloproteinase's (MMPs). 23,24 The role of tenascin in tumours growth and progression is still controversial.…”

Section: Discussionmentioning

confidence: 99%

Myofibroblastic stromal reaction and expression of tenascin-C and laminin in prostate adenocarcinoma

Tomas

Ulamec

Hudolin

et al. 2006

Prostate Cancer Prostatic Dis

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The aim of this study was to analyse relationship between changes of the stroma and expression of tenascin-C (TN-C) and laminin in prostate carcinoma. Tenascin-C immunostaining was increased, and laminin decreased in carcinomas compared with peritumoural tissue and benign prostate hyperplasia (Po0.05). Statistical analysis confirmed connection between stromal changes and TN-C expression in prostate carcinoma (Po0.05). Gleason pattern 3 carcinomas showed more pronounced stromal reaction and TN-C expression compared with Gleason pattern 4 carcinomas (Po0.05). The main cells in prostate cancer stroma are myofibroblasts that are also responsible for tenascin production. Degradation of laminin was not connected with myofibroblastic stromal changes.

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“…Fibroblasts affect the invasiveness of gastric cancer cells [20][21][22][23]. TGFβ produced from fibroblasts increases the invasiveness of scirrhous gastric cancer cells [24].…”

Section: Migration-stimulating Activity Of Gastric Cancer Cells By Fimentioning

confidence: 99%

Cancer–Stromal Interactions in Scirrhous Gastric Carcinoma

Yashiro

Hirakawa

2010

Cancer Microenvironment

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Fibroblasts play an important role in the progression, growth and spread of gastric cancers. Cancer-stroma interactions have been especially evident in the scirrhous type of gastric carcinoma. Fibroblasts are associated with the cancer progression at the primary and metastatic site. The proliferative and invasive ability of scirrhous gastric cancer cells are closely associated with the growth factors produced by organ-specific fibroblasts. Fibroblasts are therefore a key determinant in the malignant progression of gastric cancer and represent an important target for cancer therapies.

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Role of tissue stroma in cancer cell invasion

Cited by 925 publications

References 242 publications

Global analysis of host tissue gene expression in the invasive front of colorectal liver metastases

Global analysis of host tissue gene expression in the invasive front of colorectal liver metastases

Myofibroblastic stromal reaction and expression of tenascin-C and laminin in prostate adenocarcinoma

Cancer–Stromal Interactions in Scirrhous Gastric Carcinoma

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