Increased expression of matrix metalloproteinase‐2 and 9 and human papilloma virus infection are associated with malignant transformation of sinonasal inverted papilloma

Katori, Hideaki; Nozawa, Akio; Tsukuda, Mamoru

doi:10.1002/jso.20386

Cited by 34 publications

(37 citation statements)

References 11 publications

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“…The MMP-9 gene is encoded on chromosome 20 and its expression is under the control of a 2.2-kb upstream regulatory sequence harboring binding sites for AP-1, NF-B, Sp1, and others (5). MMP-9 expression is increased in malignant cancers when compared with benign tumors and non-invasive ones, and there is compelling in vitro and in vivo evidence for a role of MMP-9 in tumor invasion and angiogenesis (6,7). Its dramatic overexpression in cancer and various inflammatory conditions suggest that this protease is a potential target for the development of novel therapeutic interventions (8).…”

Section: Matrix Metalloproteinases (Mmps)mentioning

confidence: 99%

Fibronectin Increases Matrix Metalloproteinase 9 Expression through Activation of c-Fos via Extracellular-regulated Kinase and Phosphatidylinositol 3-Kinase Pathways in Human Lung Carcinoma Cells

Han

Ritzenthaler

Sitaraman

et al. 2006

Journal of Biological Chemistry

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Matrix metalloproteinases (MMPs) 2 are a family of zinc enzymes responsible for degradation of extracellular matrix components including basement membrane collagen, interstitial collagens, fibronectin (FN), and various proteoglycans during normal remodeling and repair processes (1, 2). The potent proteolytic activities of MMPs are mainly regulated by the concomitant expression of specific tissue inhibitors of matrix metalloproteinases (3). Excessive or inappropriate expression of MMPs may contribute to the pathogenesis of tissue destructive processes in a wide variety of diseases including lung disorders like bronchial asthma, chronic obstructive pulmonary disease, acute lung injury, pulmonary hypertension, and interstitial lung diseases (2, 4). In addition, MMPs have been implicated in the progression and metastases of different tumors including lung cancer (see later in text).One member of the MMP family is the 92-kDa type IV collagenase MMP-9. The MMP-9 gene is encoded on chromosome 20 and its expression is under the control of a 2.2-kb upstream regulatory sequence harboring binding sites for AP-1, NF-B, Sp1, and others (5). MMP-9 expression is increased in malignant cancers when compared with benign tumors and non-invasive ones, and there is compelling in vitro and in vivo evidence for a role of MMP-9 in tumor invasion and angiogenesis (6, 7). Its dramatic overexpression in cancer and various inflammatory conditions suggest that this protease is a potential target for the development of novel therapeutic interventions (8).Because of its perceived importance, our research focuses on the factors that increase MMP-9 expression in the lung. Our search led us to FN, a matrix glycoprotein highly expressed in tobacco-related lung disease that has been shown to stimulate lung carcinoma cell growth through several mechanisms (9 -11). Cell adhesion to FN results in MMP secretion in normal and tumor cell systems (12)(13)(14). These studies suggest that tumor cell interactions with FN might lead to MMP-9 expression thereby promoting cancer cell migration, invasion, and related processes. However, the mechanisms by which FN stim-* This work was supported by American Lung Association Bioresearch Grant RG-10215N (to S. W. H.) and by a Merit Review Grant from the Department of Veterans Affairs (to J. R.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C.

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Section: Matrix Metalloproteinases (Mmps)mentioning

confidence: 99%

Fibronectin Increases Matrix Metalloproteinase 9 Expression through Activation of c-Fos via Extracellular-regulated Kinase and Phosphatidylinositol 3-Kinase Pathways in Human Lung Carcinoma Cells

Han

Ritzenthaler

Sitaraman

et al. 2006

Journal of Biological Chemistry

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“…Epstein-Barr virus (International Agency for Research on Cancer, 1997) and human papilloma virus infections (Katori et al, 2006) have also been implicated.…”

Section: Human Effects Of Rodent Nasal Carcinogensmentioning

confidence: 99%

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

2006

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Toxicity and carcinogenicity in the mucosa of the nasal passages in rodents has been produced by a variety of organic chemicals which are systemically distributed. In this review, 14 such chemicals or classes were identified that produced rodent nasal cytotoxicity, but not carcinogenicity, and 11 were identified that produced nasal carcinogenicity. Most chemicals that affect the nasal mucosa were either concentrated in that tissue or readily activated there, or both. All chemicals with effects in the nasal mucosa that were DNA-reactive, were also carcinogenic, if adequately tested. None of the rodent nasal cytotoxins has been identified as a human systemic nasal toxin. This may reflect the lesser biotransformation activity of human nasal mucosa compared to rodent and the much lower levels of human exposures. None of the rodent carcinogens lacking DNA reactivity has been identified as a nasal carcinogen or other cancer hazard to humans. Some DNA-reactive rodent carcinogens that affect the nasal mucosa, as well as other tissues, have been associated with cancer at various sites in humans, but not the nasal cavity. Thus, findings in only the rodent nasal mucosa do not necessarily predict either a toxic or carcinogenic hazard to that tissue in humans.

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“…Significant increase of matrix metalloproteinase (MMP)-2 and 9 were also observed in IP with moderate and severe dysplasia [9]. Fascin over-expression in high-grade dysplastic epithelium in sinonasal IP may also correlate to EMMPRIN.…”

Section: Discussionmentioning

confidence: 99%

“…Various changes in protein expression have been described in dysplastic and transformed IP including increased matrix metalloproteinase (MMP)-2 and 9 [9], aberrant p53 up-regulated p21, p27, p16, and MIB 1 labeling index [4]. Further, expression of the gene p63, which bears a strong homology to the gene p53, correlates with the proliferation index in IP [10].…”

Section: Introductionmentioning

confidence: 99%

Fascin Over Expression is Associated with Dysplastic Changes in Sinonasal Inverted Papillomas: A Study of 47 Cases

Zafar

Huan

et al. 2009

Head and Neck Pathol

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Sinonasal inverted papilloma (IP) is a primary benign lesion with a tendency for local recurrence. Malignant transformation may develop in up to 15% of cases. Fascin (Fascin 1) is an actin cross-link binding protein required for the formation of actin-based cell-surface protrusions and cell motility. Fascin up-regulation in lung, gastric, breast and hepatobiliary carcinomas correlates with aggressiveness and decreased survival. Here we evaluate immunohistochemical expression of fascin in 47 sinonasal IPs from 34 patients. Fascin over-expression is significantly more common in sinonasal IP with high-grade dysplasia than in those with no dysplastic or low-grade dysplastic epithelium (P = 0.0001). No significant change in fascin expression is seen with recurrence. Over expression of fascin in high-grade dysplastic epithelium in IP may be associated with tumor progression and malignant transformation.

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Increased expression of matrix metalloproteinase‐2 and 9 and human papilloma virus infection are associated with malignant transformation of sinonasal inverted papilloma

Abstract: Precancerous lesions of IP exhibited elevated levels of MMP-2 and 9 and these expression may be associated with early events in IP carcinogenesis. HPV infection would be an early event in a multistep process of malignant formation of IP.

Cited by 34 publications

References 11 publications

Fibronectin Increases Matrix Metalloproteinase 9 Expression through Activation of c-Fos via Extracellular-regulated Kinase and Phosphatidylinositol 3-Kinase Pathways in Human Lung Carcinoma Cells

Fibronectin Increases Matrix Metalloproteinase 9 Expression through Activation of c-Fos via Extracellular-regulated Kinase and Phosphatidylinositol 3-Kinase Pathways in Human Lung Carcinoma Cells

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

Fascin Over Expression is Associated with Dysplastic Changes in Sinonasal Inverted Papillomas: A Study of 47 Cases

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