Expression of matriptase correlates with tumour progression and clinical prognosis in oral squamous cell carcinoma

Cheng, Ming Fang; Huang, Maosong; Lin, Chun–Shu; Lin, Li; Lee, Herng Sheng; Jiang, Jhih Cheng; Hsia, Kan Tai

doi:10.1111/his.12361

Cited by 23 publications

(17 citation statements)

References 47 publications

(56 reference statements)

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“…Enhanced matriptase immunoreactivity in OSCC and decreased cell surface HAI‐1 in the invasive OSCC cells have been reported . A preliminary immunohistochemical analysis in this study also showed the expression of cellular matriptase in most OSCC cases, although we could not detect a statistically significant relationship between matriptase immunoreactivity and fPAR2 score (data not shown).…”

Section: Discussioncontrasting

confidence: 58%

Deregulated matriptase activity in oral squamous cell carcinoma promotes the infiltration of cancer‐associated fibroblasts by paracrine activation of protease‐activated receptor 2

Kanemaru

Yamamoto

Kawaguchi

et al. 2016

Intl Journal of Cancer

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Cancer-associated fibroblasts (CAFs) are known to contribute to cancer progression. We have reported that cell surface expression of hepatocyte growth factor activator inhibitor 1 (HAI-1) is decreased in invasive oral squamous cell carcinoma (OSCC) cells. This study examined if HAI-1-insufficiency contributes to CAF recruitment in OSCC. Serum-free conditioned medium (SFCM) from a human OSCC line (SAS) stimulated the migration of 3 human fibroblast cell lines, NB1RGB, MRC5 and KD. SFCM from HAI-1-knockdown SAS showed an additive effect on the migration of NB1RGB and MRC5, but not KD. SAS SFCM induced protease-activated receptor-2 (PAR-2) expression in NB1RGB and MRC5, but not in KD, and a PAR-2 antagonist blocked the stimulatory effect of HAI-1 knockdown on migration of the PAR-2 expressing cell lines. Moreover, HAI-1-deficient SFCM showed additive stimulatory effects on the migration of wild-type but not PAR-2-deficient mouse fibroblasts. Therefore, the enhanced migration induced by HAI-1-insufficiency was mediated by PAR-2 activation in fibroblasts. This activation resulted from the deregulation of the activity of matriptase, a PAR-2 agonist protease. HAI-1 may thus prevent CAF recruitment to OSCC by controlling matriptase activity. When HAI-1 expression is reduced on OSCC, matriptase may contribute to CAF accumulation by paracrine activation of fibroblast PAR-2. Immunohistochemical analysis of resected OSCC revealed increased PAR2-positive CAFs in 35% (33/95) of the cases studied. The increased PAR-2 positive CAFs tended to correlate with infiltrative histology of the invasion front and shorter disease-free survival of the patients.

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Section: Discussioncontrasting

confidence: 58%

Deregulated matriptase activity in oral squamous cell carcinoma promotes the infiltration of cancer‐associated fibroblasts by paracrine activation of protease‐activated receptor 2

Kanemaru

Yamamoto

Kawaguchi

et al. 2016

Intl Journal of Cancer

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“…Moreover, matriptase confers progression of established squamous cell carcinomas by recruitment of cancer‐associated fibroblasts through activation of fibroblast PAR‐2 . In accordance with these observations, high matriptase levels in head and neck squamous cell carcinoma predict poorer prognosis of the patients …”

Section: Insufficient Hai‐1/spint1 Contributes To Epithelial Carcinogsupporting

confidence: 65%

“…Experimental evidence indicates that HAI‐1/SPINT1 and HAI‐2/SPINT2‐prostasin are required for proper trafficking and regulated activation of matriptase on the cell surface. Both autoactivation and prostasin‐mediated activation have been reported for the activation of matriptase zymogen …”

Section: Hai‐1/spint1 and Hai‐2/spint2: Emerging Guardians Of Epithelmentioning

confidence: 99%

Hepatocyte growth factor activator inhibitors (HAI‐1 and HAI‐2): Emerging key players in epithelial integrity and cancer

Kataoka

Kawaguchi

Fukushima

et al. 2018

Pathology International

127

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The growth, survival, and metabolic activities of multicellular organisms at the cellular level are regulated by intracellular signaling, systemic homeostasis and the pericellular microenvironment. Pericellular proteolysis has a crucial role in processing bioactive molecules in the microenvironment and thereby has profound effects on cellular functions. Hepatocyte growth factor activator inhibitor type 1 (HAI-1) and HAI-2 are type I transmembrane serine protease inhibitors expressed by most epithelial cells. They regulate the pericellular activities of circulating hepatocyte growth factor activator and cellular type II transmembrane serine proteases (TTSPs), proteases required for the activation of hepatocyte growth factor (HGF)/scatter factor (SF). Activated HGF/SF transduces pleiotropic signals through its receptor tyrosine kinase, MET (coded by the proto-oncogene MET), which are necessary for cellular migration, survival, growth and triggering stem cells for accelerated healing. HAI-1 and HAI-2 are also required for normal epithelial functions through regulation of TTSP-mediated activation of other proteases and protease-activated receptor 2, and also through suppressing excess degradation of epithelial junctional proteins. This review summarizes current knowledge regarding the mechanism of pericellular HGF/SF activation and highlights emerging roles of HAIs in epithelial development and integrity, as well as tumorigenesis and progression of transformed epithelial cells.

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“…100,[115][116][117] Although the mechanism is unclear, EMMPRIN homophilic binding induces the expression of a number of proteases, including MMPs, cathepsin B, and urokinase plasminogen activator receptor (uPAR). 100,115,117,118 Other proteases that have been shown to contribute to HNSCC invasion include MMP-10, 66 MMP-13, 80 matriptase, 119 fibroblast activation protein, 120 and uPA/ uPAR, 117,[121][122][123][124] as well as the glycosidase heparanase.…”

mentioning

confidence: 99%

Mechanisms of Invasion in Head and Neck Cancer

Jimenez¹,

Jayakar²,

Ow³

et al. 2015

Archives of Pathology &Amp; Laboratory Medicine

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Context.-The highly invasive properties demonstrated by head and neck squamous cell carcinoma (HNSCC) are often associated with locoregional recurrence and lymph node metastasis in patients and is a key factor leading to an expected 5-year survival rate of approximately 50% for patients with advanced disease. It is important to understand the features and mediators of HNSCC invasion so that new treatment approaches can be developed.Objectives.-To provide an overview of the characteristics, mediators, and mechanisms of HNSCC invasion.Data Sources.-A literature review of peer-reviewed articles in PubMed on HNSCC invasion.Conclusions.-Histologic features of HNSCC tumors can help predict prognosis and influence clinical treatment decisions. Cell surface receptors, signaling pathways, proteases, invadopodia function, epithelial-mesenchymal transition, microRNAs, and tumor microenvironment are all involved in the regulation of the invasive behavior of HNSCC cells. Identifying effective HNSCC invasion inhibitors has the potential to improve outcomes for patients by reducing the rate of spread and increasing responsiveness to chemoradiation.

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Expression of matriptase correlates with tumour progression and clinical prognosis in oral squamous cell carcinoma

Abstract: Matriptase expression correlates with tumour progression and invasive capability in OSCC and may be an adverse prognostic marker for this cancer.

Cited by 23 publications

References 47 publications

Deregulated matriptase activity in oral squamous cell carcinoma promotes the infiltration of cancer‐associated fibroblasts by paracrine activation of protease‐activated receptor 2

Deregulated matriptase activity in oral squamous cell carcinoma promotes the infiltration of cancer‐associated fibroblasts by paracrine activation of protease‐activated receptor 2

Hepatocyte growth factor activator inhibitors (HAI‐1 and HAI‐2): Emerging key players in epithelial integrity and cancer

Mechanisms of Invasion in Head and Neck Cancer

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