Co-expression of tenascin and fibronectin in epithelial and stromal cells of benign lesions and ductal carcinomas in the human breast

Yoshida, Toshimichi; Matsumoto, Ei-ichi; Hanamura, Noriko; Kalembeyi, Ilunga; Katsuta, Koji; Ishihara, Akinori; Sakakura, Teruyo

doi:10.1002/(sici)1096-9896(199708)182:4<421::aid-path886>3.0.co;2-u

Cited by 54 publications

(41 citation statements)

References 22 publications

(28 reference statements)

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“…IL-8 is over expressed by tumors and has been related to angiogenesis, mitotic activity and metastatization (24). Yoshida et al (25) showed IL-8 expression in breast, ovary, pancreas and prostate carcinoma related to higher stage and tumor progression. It regulates metalloproteinases 2 and 9 promoting stromal infiltration and angiogenesis facilitating the metastatic progression.…”

Section: A B Cmentioning

confidence: 99%

Gene expression profile of renal cell carcinoma clear cell type

et al. 2010

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Purpose: The determination of prognosis in patients with renal cell carcinoma (RCC) is based, classically, on stage and histopathological aspects. The metastatic disease develops in one third of patients after surgery, even in localized tumors. There are few options for treating those patients, and even the new target designed drugs have shown low rates of success in controlling disease progression. Few studies used high throughput genomic analysis in renal cell carcinoma for determination of prognosis. This study is focused on the identification of gene expression signatures in tissues of low-risk, high-risk and metastatic RCC clear cell type (RCC-CCT). Materials and Methods:We analyzed the expression of approximately 55,000 distinct transcripts using the Whole Genome microarray platform hybridized with RNA extracted from 19 patients submitted to surgery to treat RCC-CCT with different clinical outcomes. They were divided into three groups (1) low risk, characterized by pT1, Fuhrman grade 1 or 2, no microvascular invasion RCC; (2) high risk, pT2-3, Fuhrman grade 3 or 4 with, necrosis and microvascular invasion present and (3) metastatic RCC-CCT. Normal renal tissue was used as control. Results: After comparison of differentially expressed genes among low-risk, high-risk and metastatic groups, we identified a group of common genes characterizing metastatic disease. Among them Interleukin-8 and Heat shock protein 70 were over-expressed in metastasis and validated by real-time polymerase chain reaction. Conclusion: These findings can be used as a starting point to generate molecular markers of RCC-CCT as well as a target for the development of innovative therapies.

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Section: A B Cmentioning

confidence: 99%

Gene expression profile of renal cell carcinoma clear cell type

et al. 2010

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“…During cancer invasion Yoshida et al, 1997) or embryonic development of mammary glands (Kalembey et al, 1997), both mesenchymal and epithelial/parenchymal cells synthesize TNC. In contrast, our present study showed that TNC production after myocardial infarction was limited to interstitial cells.…”

Section: Are Myofibroblasts a Major Source Of Tnc?mentioning

confidence: 99%

Tenascin-C Modulates Adhesion of Cardiomyocytes to Extracellular Matrix during Tissue Remodeling after Myocardial Infarction

Imanaka‐Yoshida

Hiroe

Nishikawa

et al. 2001

Laboratory Investigation

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SUMMARY: Tenascin-C (TNC), an extracellular matrix glycoprotein, plays important roles in tissue remodeling. TNC is not normally expressed in adults but reappears under pathologic conditions. The present study was designed to clarify the contribution of TNC to ventricular remodeling after myocardial infarction. We examined the expression of TNC after experimental myocardial infarction in the rat by immunohistochemistry and in situ hybridization. Within 24 hours of permanent coronary ligation, interstitial fibroblasts in the border zone started to express TNC mRNA. The expression of TNC was down-regulated on Day 7 and was no longer apparent by Day 14 after infarction. During the healing process, TNC protein and TNC-producing cells were found at the edges of the residual myocardium. Some of the TNC-producing cells were immunoreactive for ␣-smooth muscle actin. In culture, TNC increased the number of cardiomyocytes attached to laminin but inhibited the formation of focal contacts at costameres. The results indicate that during the acute phase after myocardial infarction, interstitial cells in the border zone synthesize TNC, which may loosen the strong adhesion of surviving cardiomyocytes to connective tissue and thereby facilitate tissue reorganization. (Lab Invest 2001, 81:1015-1024.T enascins constitute a family of extracellular matrix glycoproteins (Erickson, 1993). The first member found, tenascin-C (TNC), is highly expressed in embryonic tissue during morphogenesis and sparsely expressed in the adult, but reappears during wound healing, regeneration, or cancer invasion (Chiquet-Ehrismann et al, 1986). TNC is transiently expressed in distinct areas in association with active tissue remodeling. Various in vitro findings have indicated that TNC has multiple functions in the regulation of cell migration, proliferation, and apoptosis (Chung et al, 1996;Jones and Jones, 2000). TNC counterbalances cell adhesion to substrata, correlated with cytokinesis and motility, and prevents cells from adhering too tightly to other extracellular matrix proteins (Chiquet-Ehrismann, 1995;Chiquet-Ehrismann et al, 1988;Chung et al, 1996;Murphy-Ullrich et al, 1991;Prieto et al, 1992).In the heart, TNC appears only at very early stages of embryonic development and may play important roles in the differentiation of cardiomyocytes, structural organization of the myocardium, or development of coronary vessels . TNC is not normally expressed in the adult heart but reappears under various pathologic conditions such as dilated cardiomyopathy, myocarditis, or myocardial infarction (Imanaka-Yoshida et al, 1998, 2000Tamura et al, 1996;Willems et al, 1996).To understand its roles in tissue remodeling in the diseased myocardium, we examined the expression of TNC during tissue repair after experimental myocardial infarction in rats. Sequential changes in the localization of the molecule were analyzed by immunohistochemistry, and TNC-producing cells were identified by in situ hybridization (ISH) combined with immunohistochemistry. Additionally, to ...

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“…While TN-C is expressed only at very low levels in the normal mammary gland (depending on the menstrual cycle), mammary carcinoma tissues are rich sources of TN-C, which is produced by both stromal and tumor cells (Yoshida et al, 1997;Adams et al, 2002). Furthermore, normal and transformed mammary epithelial cell lines secrete TN-C (Lightner et al, 1994;Wirl et al, 1995;Dandachi et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Enhanced tenascin-C expression and matrix deposition during Ras/TGF-β-induced progression of mammary tumor cells

et al. 2004

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Overexpression of tenascin-C (TN-C) in breast carcinomas has been associated with a migratory or even invasive tumor cell phenotype. The mechanisms regulating expression and matrix deposition of TN-C in normal and cancerous breast tissues are, however, little understood. Here, we demonstrate that mouse mammary epithelial cells (EpH4) transformed by oncogenic Ha-Ras (EpRas) overexpress TN-C, which accumulates in the cytoplasm. When EpRas cells undergo epithelial-mesenchymal transition (EMT) in response to TGFb1, they secrete TN-C into the culture medium. In EpRas cells undergoing TGFb1-induced EMT in three-dimensional (3D)-collagen gel cultures, TN-C was deposited into an extracellular matrix (ECM) already containing fibronectin and perlecan. Under less physiological 2D plastic cultures, EpRas cells undergoing EMT failed to deposit TN-C into an (apparently incomplete) ECM. Ras-downstream signaling was dissected by pharmacological inhibitors and effectorspecific Ras mutants (V12S35, V12C40), specifically inhibiting or activating ERK/MAPK or PI3K signaling, respectively. We showed that TN-C overexpression required a hyperactive ERK/MAPK-signaling pathway, while elevated PI3K signaling did not enhance TN-C expression. Similarly, tumors induced by cells exhibiting hyperactive ERK/MAPK signaling showed expression of TN-C in the tumor cells themselves, while only endothelial cells expressed TN-C in tumors caused by the V12C40 mutant (incapable of EMT in vivo). Taken together, our data indicate that hyperactive ERK/MAPK signaling causes enhanced expression of TN-C, while its secretion is induced by TGFb1 and both signals cooperate in TN-C matrix deposition. Importantly, both signals also cooperate to induce EMT in vitro and tumor progression/ metastasis in vivo.

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Co-expression of tenascin and fibronectin in epithelial and stromal cells of benign lesions and ductal carcinomas in the human breast

Cited by 54 publications

References 22 publications

Gene expression profile of renal cell carcinoma clear cell type

Gene expression profile of renal cell carcinoma clear cell type

Tenascin-C Modulates Adhesion of Cardiomyocytes to Extracellular Matrix during Tissue Remodeling after Myocardial Infarction

Enhanced tenascin-C expression and matrix deposition during Ras/TGF-β-induced progression of mammary tumor cells

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