Parenchymal-stromal switching for extracellular matrix production on invasion of oral squamous cell carcinoma

Metwaly, Hamdy; Maruyama, Satoshi; Yamazaki, Manabu; Tsuneki, Masayuki; Abé, Tatsuya; Jen, Kai Yu; Cheng, Jun; Saku, Takashi

doi:10.1016/j.humpath.2012.02.006

Cited by 22 publications

(21 citation statements)

References 33 publications

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“…In conclusion, based on the present in vivo and in vitro results and lines of evidence documented in the literature, it is possible to conclude that PAR-2 is required for growth and invasion of oral SCC cells and that it is a novel immunohistochemical marker for histopathologic diagnosis of oral malignancies, in addition to those we have already established [4][5][6][7][8][9][10][11][12][13]28], especially when the differential diagnosis of CIS from epithelial dysplasia is difficult. In the next step, the molecular mechanism for PAR-2 activation in the invading front of oral SCC should be investigated more in detail to open a research field toward an anticancer therapy in which repression of PAR-2 should be targeted.…”

Section: Discussionsupporting

confidence: 60%

“…ZK-1 cells, a human carcinoma cell system, have been established from a well-differentiated SCC arising in the tongue of a 53-year-old man [12], whereas MK-1 cells, another SCC cell system with highly metastatic potential, have been established from a submandibular lymph node metastatic focus of a tongue SCC from a 57-year-old man [28]. ZK-1 and MK-1 cells were seeded in 25-mL plastic flasks at a cell concentration of 4 × 10 4 in 5 mL Dulbecco's minimal essential medium (DMEM; Gibco, Thermo Fisher Scientific, Waltham, MA) containing 10% fetal calf serum (Gibco), 50 IU/mL penicillin, and 50 μg/mL streptomycin (Gibco) and cultured at 37°C in humidified 5% carbon dioxide 95% air atmosphere.…”

Section: Cellsmentioning

confidence: 99%

“…We have also demonstrated the genetic mechanism for the loss of K13 as well as the reciprocal loss of K13 and emergence of K16/ K17 in oral CIS [5,6]. To consolidate our diagnostic criteria of oral CIS, we have introduced some other immunohistochemistry for podoplanin [7,8], perlecan [9][10][11][12], matrix metalloproteinase (MMP) 7 [10], tenascin [12], and β-catenin/E-cadherin [11] as diagnostic aids. More recently, we have also emphasized the formation of intraepithelial blood vessels as one of the histopathologic characteristics of oral CIS and as a driving force for dyskeratosis among cancer cells [13].…”

Section: Introductionmentioning

confidence: 99%

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Protease-activated receptor 2 modulates proliferation and invasion of oral squamous cell carcinoma cells

et al. 2015

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Section: Discussionsupporting

confidence: 60%

Section: Cellsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protease-activated receptor 2 modulates proliferation and invasion of oral squamous cell carcinoma cells

et al. 2015

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“…Cells and Reagents SCC cell systems (lines) (ZK-1, ZK-2, and MK-1) were established from SCC arising in the tongue (ZK-1 and ZK-2) 21 and gingiva (MK-1). 22 Salivary gland adenoid cystic carcinoma (ACC) cell systems (lines), ACC2 and ACC3, were established from ACCs of the palatal minor salivary gland and parotid gland, respectively, 23 and ACCM was subcloned from ACC2 cells as a clone with highly metastatic potential.…”

Section: Materials and Methods Clinical Samplesmentioning

confidence: 99%

Podoplanin-mediated cell adhesion through extracellular matrix in oral squamous cell carcinoma

Tsuneki

Yamazaki

Maruyama

et al. 2013

Laboratory Investigation

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Podoplanin (PDPN), one of the representative mucin-like type-I transmembrane glycoproteins specific to lymphatic endothelial cells, is expressed in various cancers including squamous cell carcinoma (SCC). On the basis of our previous studies, we have developed the hypothesis that PDPN functions in association with the extracellular matrix (ECM) from the cell surface side. The aim of this study was to elucidate the molecular role of PDPN in terms of cell adhesion, proliferation, and migration in oral SCC cells. Forty-four surgical specimens of oral SCC were used for immunohistochemistry for PDPN, and the expression profiles were correlated with their clinicopathological properties. Using ZK-1, a human oral SCC cell system, and five other cell systems, we examined PDPN expression levels by immunofluorescence, western blotting, and real-time PCR. The effects of transient PDPN knockdown by siRNA in ZK-1 were determined for cellular functions in terms of cell proliferation, adhesion, migration, and invasion in association with CD44 and hyaluronan. Cases without PDPN-positive cells were histopathologically classified as less-differentiated SCC, and SCC cells without PDPN more frequently invaded lymphatics. Adhesive properties of ZK-1 were significantly inhibited by siRNA, and PDPN was shown to collaborate with CD44 in cell adhesion to tether SCC cells with hyaluronan-rich ECM of the narrow intercellular space as well as with the stromal ECM. There was no siRNA effect in migration. We have demonstrated the primary function of PDPN in cell adhesion to ECM, which is to secondarily promote oral SCC cell proliferation.Laboratory Investigation (2013) 93, 921-932;

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“…Histopathologically, OSCC presents as fibrous connective tissue with unusual amounts of extracellular matrix rich in fibroblasts, vascular vessels, and inflammatory cells [26]. Among the local milieu of OSCC stromal spaces, rich in perlecans and inflammatory cells, monocytes or resting macrophages are differentiated into LyC16 high , CD163 + , CD204 + , and CD68 + expressing TAMs.…”

Section: Introductionmentioning

confidence: 99%

Role of tumour-associated macrophages in oral squamous cells carcinoma progression: an update on current knowledge

et al. 2017

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BackgroundOral squamous cell carcinoma (OSCC) accounts over 90% of malignant neoplasms of the oral cavity. This pathological entity is associated to a high mortality rate that has remained unchanged over the past decades. Tumour-associated macrophages (TAMs) are believed to have potential involvement in OSCC progression. However, the molecular networks involved in communication between stroma and cancer cells have not yet been fully elucidated.Main bodyThe role of M2 polarized cells in oral carcinogenesis is supported by a correlation between TAMs accumulation into OSCC stroma and poor clinical outcome. Signalling pathways such as the NF-κB and cytokines released in the tumour microenvironment promote a bidirectional cross-talk between M2 and OSCC cells. These interactions consequently result in an increased proliferation of malignant cells and enhances aggressiveness, thus reducing patients’ survival time.ConclusionsHere, we present a comprehensive review of the role of interleukin (IL)-1, IL-4, IL-6, IL-8, IL-10 and the receptor tyrosine kinase Axl in macrophage polarization to an M2 phenotype and OSCC progression. Understanding the molecular basis of oral carcinogenesis and metastatic spread of OSCC would promote the development of targeted treatment contributing to a more favourable prognosis.

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Parenchymal-stromal switching for extracellular matrix production on invasion of oral squamous cell carcinoma

Cited by 22 publications

References 33 publications

Protease-activated receptor 2 modulates proliferation and invasion of oral squamous cell carcinoma cells

Protease-activated receptor 2 modulates proliferation and invasion of oral squamous cell carcinoma cells

Podoplanin-mediated cell adhesion through extracellular matrix in oral squamous cell carcinoma

Role of tumour-associated macrophages in oral squamous cells carcinoma progression: an update on current knowledge

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