Increased invasion and matrix metalloproteinase-2 expression by Snail-induced mesenchymal transition in squamous cell carcinomas

Yokoyama, Keitaro; Kamata, Nobuyuki; Fujimoto, Ryoichi; Tsutsumi, Satoshi; Tomonari, Mayumi; Taki, Masayuki; Hosokawa, Hiroyoshi; Nagayama, Masaru

doi:10.3892/ijo.22.4.891

Cited by 136 publications

(160 citation statements)

References 0 publications

Supporting

Mentioning

136

Contrasting

Unclassified

Order By: Relevance

“…We have previously reported that oral SCC cells produce a large amount of matrix degrading enzyme, such as MMPs or uPAs (25), which might contribute to invasiveness and lymph node metastasis. During EMT, the involvement of MMPs or uPAs has been also suggested (26)(27)(28); however, we could not find significant alteration of MMP-2, MMP-7 and uPA by treatment with SDF-1. Scotton et al showed that the invasion of ovarian cancer cells through Matrigel stimulated by SDF-1 inhibited the presence of the MMP inhibitor, marimastat, but that no MMPs or tissue inhibitors of metalloproteinases (TIMPs) appeared to be regulated by SDF-1 (29).…”

Section: Discussioncontrasting

confidence: 53%

Epithelial-mesenchymal transition induced by the stromal cell-derived factor-1/CXCR4 system in oral squamous cell carcinoma cells

Onoue

Uchida²,

Begum³

et al. 2006

Int J Oncol

View full text Add to dashboard Cite

Abstract. Epithelial-mesenchymal transition (EMT) refers to critical events occasionally observed during tumor progression, including invasion and metastasis, by which cancer cells acquire a fibroblast-like phenotype. Since the stromal cellderived factor-1 (SDF-1)/CXCR4 system can facilitate lymph node metastasis in oral squamous cell carcinoma (SCC), we have explored the possibility that this system might be involved in EMT. Oral SCC cells, B88 and HNt, which have functional CXCR4 and lymph node metastatic potential, were found to lose their epithelial cell morphology due to SDF-1. In this context, the downregulation of epithelial markers, cytokeratin, E-cadherin and ß-catenin, and the upregulation of mesenchymal marker, vimentin and snail were detected. Furthermore, upregulation of vimentin by treatment with SDF-1 was impaired by phosphatidylinositol 3 kinase (PI3K) inhibitor Wortmannin, but not by mitogenactivated protein kinase/extracellular signal-regulated kinase inhibitor U0126. In the type I collagen embedding culture, SDF-1-treated B88 cells formed protruding extensions, but the effect was impaired by treatment with Wortmannin. These results suggested that EMT induced by the SDF-1/ CXCR4 system might be involved in the lymph node metastasis of oral SCCs via activation of PI3K-Akt/PKB pathway.

show abstract

Section: Discussioncontrasting

confidence: 53%

Epithelial-mesenchymal transition induced by the stromal cell-derived factor-1/CXCR4 system in oral squamous cell carcinoma cells

Onoue

Uchida²,

Begum³

et al. 2006

Int J Oncol

View full text Add to dashboard Cite

show abstract

“…Accumulating data now also show that these factors can modulate the expression of other genes implicated in tumor cell invasion. For instance, they have been shown to downregulate other cell-cell contact molecules but also to upregulate 'mesenchymal' genes including fibronectin, vimentin and members of the matrix metalloproteases (MMP) family (Savagner et al, 1997;Cano et al, 2000;Hajra et al, 2002;Bolos et al, 2003;Ikenouchi et al, 2003;Yokoyama et al, 2003;Ohkubo and Ozawa, 2004;Vandewalle et al, 2005). Much less is known regarding the δEF1/ZEB family.…”

Section: Discussionmentioning

confidence: 99%

Regulation of vimentin by SIP1 in human epithelial breast tumor cells

et al. 2006

View full text Add to dashboard Cite

The expression of Smad interacting protein-1 (SIP1; ZEB2) and the de novo expression of vimentin are frequently involved in epithelial-to-mesenchynial transitions (EMTs) under both normal and pathological conditions. In the present study, we investigated the potential role of SIP1 in the regulation of vimentin during the EMT associated with breast tumor cell migration and invasion. Examining several breast tumor cell Unes displaying various degrees of invasiveness, we found SIP1 and vimentin expression only in invasive cell Unes. Also, using a model of cell migration with human mammary MCF10A cells, we showed that SIP1 is induced specifically in vimentin-positive migratory cells. Furthermore, transfection of SIP1 cDNA in MCF10A cells increased their vimentin expression both at the mRNA and protein levels and enhanced their migratory abilities in Boyden Chamber assays. Inversely, inhibition of SIP1 expression by RNAi strategies in BT-549 cells and MCF10A cells decreased vimentin expression. We also showed that SIP1 transfection did not activate the TOP-FLASH reporter system, suggesting that the β-catenin/ TCF pathway is not impUcated in the regulation of vimentin by SIP1. Our results therefore impUcate SIP1 in the regulation of vimentin observed in the EMT associated with breast tumor cell migration, a pathway that may contribute to the metastatic progression of breast cancer.

show abstract

“…Western blotting analysis was performed as previously reported. 32) Cell lysate was denatured at 100°C for 5 min, separated by SDS-polyacrylamide gel electrophoresis and transferred onto a nitrocellulose membrane (Bio-Rad, Richmond, CA). The membrane was incubated with a blocking buffer consisting of 5% skimmed milk and 1% bovine serum albumin in TBST (137 mM NaCl, 2.68 mM KCl, 0.1% Tween-20, 25 mM Tris-HCl, pH 7.5) for 3 h and with a rat monoclonal anti-HA, clone 3F10 (Roche, Mannheim, Germany) overnight, followed by horseradish peroxidase-conjugated goat anti-rat IgG (Sigma).…”

Section: )mentioning

confidence: 99%

Downregulation of Wnt4 and upregulation of Wnt5a expression by epithelialmesenchymal transition in human squamous carcinoma cells

et al. 2003

Self Cite

View full text Add to dashboard Cite

show abstract

Increased invasion and matrix metalloproteinase-2 expression by Snail-induced mesenchymal transition in squamous cell carcinomas

Cited by 136 publications

References 0 publications

Epithelial-mesenchymal transition induced by the stromal cell-derived factor-1/CXCR4 system in oral squamous cell carcinoma cells

Epithelial-mesenchymal transition induced by the stromal cell-derived factor-1/CXCR4 system in oral squamous cell carcinoma cells

Regulation of vimentin by SIP1 in human epithelial breast tumor cells

Downregulation of Wnt4 and upregulation of Wnt5a expression by epithelialmesenchymal transition in human squamous carcinoma cells

Contact Info

Product

Resources

About