Epigenetic Loss of Mucosa-Associated Lymphoid Tissue 1 Expression in Patients with Oral Carcinomas

Chiba, Takehiko; Maeda, Genta; Kawashiri, Shin‐ya; Kato, Koroku; Imai, Kazushi

doi:10.1158/0008-5472.can-09-1140

Cited by 15 publications

(20 citation statements)

References 39 publications

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“…Aggressive subsets of oral SCC cells frequently lose the keratinocyte-differentiation markers and express mesenchymal cell-specific molecules at the invasive front [28]–[32]. This indicates the presence and involvement of EMT in the carcinoma progression.…”

Section: Discussionmentioning

confidence: 99%

Progression of Oral Squamous Cell Carcinoma Accompanied with Reduced E-Cadherin Expression but Not Cadherin Switch

et al. 2012

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The cadherin switch from E-cadherin to N-cadherin is considered as a hallmark of the epithelial-mesenchymal transition and progression of carcinomas. Although it enhances aggressive behaviors of adenocarcinoma cells, the significance and role of cadherin switch in squamous cell carcinomas (SCCs) are largely controversial. In the present study, we immunohistochemically examined expression of E-cadherin and N-cadherin in oral SCCs (n = 63) and its implications for the disease progression. The E-cadherin-positive carcinoma cells were rapidly decreased at the invasive front. The percentage of carcinoma cells stained E-cadherin at the cell membrane was reduced in parallel with tumor dedifferentiation (P<0.01) and enhanced invasion (P<0.01). In contrast, N-cadherin-positive cells were very limited and did not correlate with the clinicopathological parameters. Mouse tongue tumors xenotransplantated oral SCC cell lines expressing both cadherins in vitro reproduced the reduction of E-cadherin-positive carcinoma cells at the invasive front and the negligible expression of N-cadherin. These results demonstrate that the reduction of E-cadherin-mediated carcinoma cell-cell adhesion at the invasive front, but not the cadherin switch, is an important determinant for oral SCC progression, and suggest that the environments surrounding carcinoma cells largely affect the cadherin expression.

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Section: Discussionmentioning

confidence: 99%

Progression of Oral Squamous Cell Carcinoma Accompanied with Reduced E-Cadherin Expression but Not Cadherin Switch

et al. 2012

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“…HSC2 cells stably expressing FLAG-tagged full-length wild-type MALT1 ( wtMALT1 HSC2 cells) and the NH 2 terminal death and Ig-like domains-deleted dominant-negative MALT1 ( ΔMALT1 HSC2 cells; Che et al , 2004) and transfected vector alone ( mock HSC2 cells) were established previously (Chiba et al , 2009). They were maintained in 10% fetal bovine serum and 100 units per ml of penicillin/streptomycin-containing DMEM (Sigma-Aldrich, St. Louis, MO, USA) in a conventional 5% CO 2 incubator.…”

Section: Methodsmentioning

confidence: 99%

“…Our previous study demonstrated that mucosa-associated lymphoid tissue 1 (MALT1) is expressed in the nucleus of oral epithelial cells (Chiba et al , 2009) and substitutes keratins depending on its expression (Kawamoto et al , 2013). The advanced carcinomas inactivate MALT1 expression by the promoter methylation, and the loss of expression worse the patient prognosis (Chiba et al , 2009). However, nothing is known about the role of loss of expression in the carcinoma progression at present.…”

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confidence: 99%

Inhibition of TGF-β and EGF pathway gene expression and migration of oral carcinoma cells by mucosa-associated lymphoid tissue 1

et al. 2013

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Background:Expression of mucosa-associated lymphoid tissue 1 (MALT1) is inactivated in oral carcinoma patients with worse prognosis. However, the role in carcinoma progression is unknown. Unveiling genes under the control of MALT1 is necessary to understand the pathology of carcinomas.Methods:Gene data set differentially transcribed in MALT1-stably expressing and -marginally expressing oral carcinoma cells was profiled by the microarray analysis and subjected to the pathway analysis. Migratory abilities of cells in response to MALT1 were determined by wound-healing assay and time-lapse analysis.Results:Totally, 2933 genes upregulated or downregulated in MALT1-expressing cells were identified. The subsequent pathway analysis implicated the inhibition of epidermal growth factor and transforming growth factor-β signalling gene expression, and highlighted the involvement in the cellular movement. Wound closure was suppressed by wild-type MALT1 (66.4%) and accelerated by dominant-negative MALT1 (218.6%), and the velocities of cell migration were increased 0.2-fold and 3.0-fold by wild-type and dominant-negative MALT1, respectively.Conclusion:These observations demonstrate that MALT1 represses genes activating the aggressive phenotype of carcinoma cells, and suggest that MALT1 acts as a tumour suppressor and that the loss of expression stimulates oral carcinoma progression.

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“…Since proteolytic degradation of the extracellular matrix releases growth factors (38), we should consider the impact of carcinoma cell-tissue interactions on the expression carefully. Furthermore, an intracellular signaling molecule, mucosa-associated lymphoid tissue 1, which suppresses the aggressive phenotype of oral carcinoma cells and is inactivated in the patients with worse prognosis directly affects FABP expression (39,40). Therefore both genetic and environmental factors provoke carcinoma cells to express FABP5.…”

Section: Discussionmentioning

confidence: 99%

Differential expression of fatty acid-binding proteins and pathological implications in the progression of tongue carcinoma

Ohyama

Kawamoto

Chiba

et al. 2013

Molecular and Clinical Oncology

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Abstract. Tongue carcinomas are common malignancies of the oral cavity. Understanding the molecular mechanisms behind the disease progression is a prerequisite for improving patient prognosis. Fatty acid-binding proteins (FABPs) are cytoplasmic lipid chaperones that affect cellular organization and energy production. Although their aberrant expression is involved in carcinoma progression, its role in the pathology of tongue carcinomas remains unclear. In the present study, the immunohistochemical expression of FABP4 and FABP5 in tongue carcinomas (n=58) and its involvement in the clinicopathological parameters were examined. Normal tongue epithelial cells expressed FABP5, an epidermal-type FABP, but not FABP4, an adipocyte-type FABP. The cytoplasmic staining of FABP5 was increased in carcinomas with advanced T-stage (P<0.05) and clinical stage (P<0.05). Ectopic expression of FABP4 was detected in almost all carcinomas, although its role in disease progression remains undetermined. Upregulation of FABP5 in the wounded skin of genetically normal mice indicated that microenvironmental tissue factors induce FABP5 expression. The results of the present study demonstrated the aberrant expression of FABP4 and FABP5 in tongue carcinomas and suggested the involvement of FABP5 in disease progression.

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Epigenetic Loss of Mucosa-Associated Lymphoid Tissue 1 Expression in Patients with Oral Carcinomas

Cited by 15 publications

References 39 publications

Progression of Oral Squamous Cell Carcinoma Accompanied with Reduced E-Cadherin Expression but Not Cadherin Switch

Progression of Oral Squamous Cell Carcinoma Accompanied with Reduced E-Cadherin Expression but Not Cadherin Switch

Inhibition of TGF-β and EGF pathway gene expression and migration of oral carcinoma cells by mucosa-associated lymphoid tissue 1

Differential expression of fatty acid-binding proteins and pathological implications in the progression of tongue carcinoma

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