Tenascin-C Expression and Its Prognostic Significance in Colorectal Cancer

Lundin, Mikael; Nordling, Stig; Lundin, Johan; Haglund, Caj

doi:10.1159/000113490

Cited by 11 publications

(9 citation statements)

References 62 publications

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“…Tenascin expression is highly upregulated during tumor invasion in many tumor types, including colorectal carcinomas [24]. In the present study we found a borderline relationship of TSP-1 expression with TN (p=0.053).…”

Section: Discussionsupporting

confidence: 40%

“…In infiltrating CRC, TN is expressed in the stroma and appears to be associated with progressive disease and poor prognosis [23]. FN is regarded as the major mesenchymal ECM glycoprotein involved in cell-matrix and cell-cell adhesion, cell migration, morphogenesis, differentiation, and oncogene transformation [24]. In CRC, FN immunostain shown a strong expression and different distribution compared with normal colorectal tissue [23,24].…”

Section: Introductionmentioning

confidence: 99%

“…FN is regarded as the major mesenchymal ECM glycoprotein involved in cell-matrix and cell-cell adhesion, cell migration, morphogenesis, differentiation, and oncogene transformation [24]. In CRC, FN immunostain shown a strong expression and different distribution compared with normal colorectal tissue [23,24]. Collagen type IV (Coll IV), constitute the major intrinsic component of basement membrane (BM) and is involved in cellular adhesion to BM and the extracellular matrix [25].…”

Section: Introductionmentioning

confidence: 99%

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Association Between Thrombospondin-1, Angiogenesis Related Markers, and Extracellular Matrix Components with Colorectal Cancer Outcome

Mitselou¹,

Arvanitis²,

Skoufi³

et al. 2013

TOCOLCJ

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Abstract:Background: Angiogenesis is a multistep process that depends on the balance of proangiogenic factors and inhibitors as well as on interactions with the extracellular matrix. Thrombospondin-1 (TSP-1) is an endogenous inhibitor of angiogenesis encoded by THBS1 gene, whose promoter is activated by p53. Aim:To evaluate the relevance of TSP-1 in patients with colorectal cancer. Material and Methods:We examined the immunohistochemical expression of angiogenic agents (VEGF and CD34), proliferation associated indices, extracellular matrix components (tenascin, fibronectin, laminin, and collagen type IV), and the antiangiogenic agent TPS-1 in 97 patients with colorectal carcinoma (CRC) and correlated their expression levels with clinicopathological parameters.Results: TSP-1 was detected in the tumor cells, stroma and perivascular tissue. High and moderate tumor TSP-1 expression was observed in 24.75%, weak in 19.6%, while 55.7% of the cases were negative. High stromal expression was observed in 40.2% and perivascular stain was noted in 31.95% of the cases. Stromal TSP-1 expression was correlated with tumor type and tumor grade (p=0.001, and p=0.041 respectively) and with ECM components expression: tenascin (p=0.053), fibronectin (p=0.063), collagen type IV (p=0.004) and laminin (p=0.0001). The relationship of TSP-1 expression with tumor angiogenesis, growth fraction, p53 protein expression, and overall survival was not significant. Conclusions:Our data suggest that both tumor and stromal TSP-1 expression may not be a direct antiangiogenic factor, although it seems to be implicated in the remodeling of colorectal cancer tissue through interaction with other extracellular matrix components.

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Section: Discussionsupporting

confidence: 40%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Association Between Thrombospondin-1, Angiogenesis Related Markers, and Extracellular Matrix Components with Colorectal Cancer Outcome

Mitselou¹,

Arvanitis²,

Skoufi³

et al. 2013

TOCOLCJ

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“…No fibronectin was detected in MCF-7 or MDA-IBC-3 mammospheres. Tenascin-C is expressed in the stroma of tumors and is associated with a poor prognosis [20], [21]. Tenascin-C binds to fibronectin and can reduce cell adhesion in vitro [22].…”

Section: Resultsmentioning

confidence: 99%

Mesenchymal Stem Cells Promote Mammosphere Formation and Decrease E-Cadherin in Normal and Malignant Breast Cells

et al. 2010

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IntroductionNormal and malignant breast tissue contains a rare population of multi-potent cells with the capacity to self-renew, referred to as stem cells, or tumor initiating cells (TIC). These cells can be enriched by growth as “mammospheres” in three-dimensional cultures.ObjectiveWe tested the hypothesis that human bone-marrow derived mesenchymal stem cells (MSC), which are known to support tumor growth and metastasis, increase mammosphere formation.ResultsWe found that MSC increased human mammary epithelial cell (HMEC) mammosphere formation in a dose-dependent manner. A similar increase in sphere formation was seen in human inflammatory (SUM149) and non-inflammatory breast cancer cell lines (MCF-7) but not in primary inflammatory breast cancer cells (MDA-IBC-3). We determined that increased mammosphere formation can be mediated by secreted factors as MSC conditioned media from MSC spheroids significantly increased HMEC, MCF-7 and SUM149 mammosphere formation by 6.4 to 21-fold. Mammospheres grown in MSC conditioned media had lower levels of the cell adhesion protein, E-cadherin, and increased expression of N-cadherin in SUM149 and HMEC cells, characteristic of a pro-invasive mesenchymal phenotype. Co-injection with MSC in vivo resulted in a reduced latency time to develop detectable MCF-7 and MDA-IBC-3 tumors and increased the growth of MDA-IBC-3 tumors. Furthermore, E-cadherin expression was decreased in MDA-IBC-3 xenografts with co-injection of MSC.ConclusionsMSC increase the efficiency of primary mammosphere formation in normal and malignant breast cells and decrease E-cadherin expression, a biologic event associated with breast cancer progression and resistance to therapy.

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“…TN‐c appeared in the ECM as a continuous line or as reticulate yellow grains. The level of immunoreactivity was expressed by scoring the intensity of TN staining (2). No color or light staining was considered negative, while yellow or yellow‐brown staining was considered positive.…”

Section: Methodsmentioning

confidence: 99%

Integrin β3 and its ligand regulate the expression of uPA through p38 MAPK in breast cancer

Wang

Han

et al. 2010

APMIS

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Interplay between integrins and extracellular matrix is suggested to play an important role in malignant progression and tumor differentiation. The aim of the study was to determine the combined expression of integrin β3 and tenascin-c (TN-c) in breast cancer and examine whether integrin β3 and TN-c can activate urokinase-type plasminogen activator (uPA) through p38 mitogen-activated protein kinase (p38 MAPK). We detected the expression of integrin β3, TN-c, p-p38, and uPA in 80 cases of breast invasive ductal carcinoma by immunohistochemistry. In addition, we blocked integrin β3 and TN-c in the MDA-MB-231 breast cancer cells and detected the expression of p-p38 and uPA by Western blot. Integrin β3, TN-c, p-p38, and uPA showed high levels of expression in breast invasive ductal carcinoma. The expression of integrin β3, TN-c, and uPA was correlated with lymph node metastasis and TNM stage in breast cancer. Furthermore, correlations were noted between any two of the three proteins. The expression of p-p38 and uPA decreased in MDA-MB-231 cells after the addition of integrin β3 antibody and TN-c antibody. The expression of uPA decreased after addition of SB203580. Our results demonstrate that inhibition of the expression of integrin β3 and TN-c could decrease the expression of uPA through p38 MAPK in breast cancer, suggesting that the interaction between integrin β3 and TN-c serves an important role in breast cancer.

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Tenascin-C Expression and Its Prognostic Significance in Colorectal Cancer

Cited by 11 publications

References 62 publications

Association Between Thrombospondin-1, Angiogenesis Related Markers, and Extracellular Matrix Components with Colorectal Cancer Outcome

Association Between Thrombospondin-1, Angiogenesis Related Markers, and Extracellular Matrix Components with Colorectal Cancer Outcome

Mesenchymal Stem Cells Promote Mammosphere Formation and Decrease E-Cadherin in Normal and Malignant Breast Cells

Integrin β3 and its ligand regulate the expression of uPA through p38 MAPK in breast cancer

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