Activation of Smad signaling enhances collagenase-3 (MMP-13) expression and invasion of head and neck squamous carcinoma cells

Leivonen, Suvi‐Katri; Ala-aho, Risto; Koli, Katri; Grénman, Reidar; Peltonen, Juha; Kähäri, Veli‐Matti

doi:10.1038/sj.onc.1209291

Cited by 89 publications

(82 citation statements)

References 58 publications

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“…32 SDF-1 binding to CXCR4 can activate Akt, 34 transactivate epidermal growth factor receptor, 35 activate JAK2/STAT3 leading to enhanced survival and inhibition of apoptosis 36 and alter ras signaling. 37 SDF-1 signaling also induces production of the matrix metalloproteinases MMP-2, MMP-9 38 and MMP-13 39 that are important for breaking down basement membrane.…”

Section: Discussionmentioning

confidence: 99%

Dynamic stromal‐epithelial interactions during progression of MCF10DCIS.com xenografts

Tait

Pauley

Santner

et al. 2007

Intl Journal of Cancer

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cells form comedo type ductal carcinoma in situ in immune-deficient mice before forming invasive ductal carcinoma. As the lesions mature, both stromal and epithelial cells undergo phenotypic changes detected by immunohistochemistry. Myofibroblasts are present before the formation of carcinoma in situ and after development of invasive carcinoma. MCF10DCIS. com lesions develop a myoepithelial layer prior to exhibiting a basement membrane surrounding the ductal mass. TGFb1 is initially expressed by the epithelial cells but is expressed by stroma in invasive carcinoma. Stromal derived factor-1 is detected in epithelial cells in early carcinoma in situ but is produced in stromal cells in invasive carcinoma. The receptor CXCR4 is expressed by epithelial cells in the xenografts at all times, as is the hepatocyte growth factor receptor c-met. MCF10DCIS.com xenografts illustrate the dynamic interplay of epithelium and stroma in the development of carcinoma in situ and subsequent invasive carcinoma. Although the phenotype of the epithelial cells may be dependent upon the stroma, the malignant epithelium induces the development of the stroma necessary for progression to the invasive stage. ' 2007 Wiley-Liss, Inc.Key words: breast cancer; carcinoma in situ; MCF10DCIS.com; progression; stroma; xenograft The natural history of cancer is thought to involve multiple sequential genetic changes including mutations, loss of heterozygosity and amplification of gene copy number as well as epigenetic changes such as hypermethylation of promoter regions. In many epithelial cancers a series of abnormal histologic changes can be identified and associated with increased risk of progressing to malignant disease. It has been assumed that each stage accumulates additional genetic anomalies. The first recognized lesion with increased risk for breast cancer is hyperplasia ( a 4-fold increased risk for atypical ductal hyperplasia) but genetic anomalies are rare. ErbB2 is rarely detected in benign lesions. 1-3 However, overexpression of erbB2 is frequent in DCIS and IDC. Studies of mixed lesions, containing both in situ and invasive components, invariably report that the 2 components express erbB2 coordinately. 4-6 A similar pattern occurs for cyclin D1 expression; rare in benign hyperplastic lesions but frequent in both DCIS and IDC and expressed coordinately in both in situ and invasive components of mixed lesions. 7,8 Recent studies suggest that nearly all genetic alterations have occurred by the time of DCIS formation. Comparative genomic hybridization analysis of breast DCIS and IDC found no significant difference in the number of chromosomal abnormalities, although the frequency of a few specific changes varied in high grade versus low grade DCIS and between DCIS and concurrent IDC. 9 A more recent study confirmed that DCIS is genetically advanced. Allelic imbalance of 52 microsatellite markers of chromosomal regions commonly lost in breast cancer increased significantly between atypical ductal hyperplasia and DCIS but not between DCIS an...

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Section: Discussionmentioning

confidence: 99%

Dynamic stromal‐epithelial interactions during progression of MCF10DCIS.com xenografts

Tait

Pauley

Santner

et al. 2007

Intl Journal of Cancer

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“…The MMPs can be divided into subgroups of collagenases, gelatinases, stromelysins, matrilysins, membrane-type MMPs, and other MMPs according to their substrate specificity and function (Yong et al 2001). MMP-13 is a collagenolytic MMP characterized by a wide substrate specificity, and it is expressed by many types of invasive tumors, such as breast carcinomas (Freije et al 1994), squamous cell carcinomas of the head and neck (Leivonen et al 2006). The correlation between MMP-13 expression level and invasive capacity suggests that MMP-13 is an important molecule for cancer progression.…”

Section: Introductionmentioning

confidence: 99%

Leptin induces migration and invasion of glioma cells through MMP‐13 production

Yeh

Lee

et al. 2008

Glia

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Leptin, the product of the obses gene, plays an important role in the regulation of body weight by coordinating metabolism, feeding behavior, energy balance and neuroendocrine responses. However, central regulation of leptin gene expression is different from that in the adipocytes. In addition, leptin has been found in many tumor cell lines and has been shown to have mitogenic and angiogenic activity in a number of cell types. Glioma is the most common primary adult brain tumor with poor prognosis due to the spreading of tumor cell to the other regions of brain easily. Here we found that malignant C6 glioma cells expressed more leptin and leptin receptors than non-malignant astrocytes. Furthermore, it was found that exogenous application of leptin enhanced the migration and invasion of C6 glioma cells. In addition, we found that the expression of matrix metalloproteinase-13 (MMP-13) but not of MMP-2 and MMP-9 was increased in response to leptin stimulation. The leptin-induced increase of cell migration and invasion was antagonized by MMP-13 neutralizing antibody or silencing MMP-13. The up-regulation of MMP-13 induced by leptin was mainly through p38 MAP kinase and NF-κB pathway. In addition, migration-prone sublines demonstrate that cells with increasing migration ability had more expression of MMP-13 and leptin. Taken together, these results indicate that leptin enhanced migration and invasion of C6 glioma cells through the increase of 2

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“…Increased expression of VEGF is seen in OSCC through all stages of disease progression [106][107][108]. Other factors that promote blood vessel formation and endothelial cell migration include, prostaglandin E2 (PGE 2 ) and TGF-β̣ are often overexpressed by tumor cells [109][110][111][112][113]. COX-2 inhibition has been shown to be effective in controlling OSCC cell proliferation and this is shown to be mediated specifically through the inhibition of PGE 2 .…”

Section: Cdk2ap1-also Known As P12mentioning

confidence: 99%

Molecular mechanisms of head and neck cancer

Deshpande

Wong²

2008

Expert Review of Anticancer Therapy

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Background-With a global incidence rank of eight and a significant portion of head and neck malignancies (~90%), oral squamous cell carcinoma (OSCC) poses a major health risk and is one of the leading cause of mortality in developing nations [1]. Distribution of the incidence of OSCC varies across the world with south-central Asia and Africa leading, followed by eastern and central Europe, and to a lesser extent Australia, Japan, and the United States. Over the past few years there has been a drastic increase in the incidence of oral cancer in most parts of the world [2]. In the United States alone, with about 17 new cases/100,000, oral cancer is the fifth most common and sixth leading cause of cancer-related mortality per year [3].While men tend to have a higher incidence of OSCC (6.6/100,000) compared to women (2.9/100,000), there is an equal mortality rate between the sexes (50%).

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Activation of Smad signaling enhances collagenase-3 (MMP-13) expression and invasion of head and neck squamous carcinoma cells

Abstract: Squamous cell carcinoma (SCC) cells of the head and neck specifically express collagenase-3 (matrix metalloproteinase-13 (MMP-13)), the expression of which correlates with their invasion capacity. Transforming

Cited by 89 publications

References 58 publications

Dynamic stromal‐epithelial interactions during progression of MCF10DCIS.com xenografts

Dynamic stromal‐epithelial interactions during progression of MCF10DCIS.com xenografts

Leptin induces migration and invasion of glioma cells through MMP‐13 production

Molecular mechanisms of head and neck cancer

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