E-Cadherin truncation and Sialyl Lewis-X overexpression in oral squamous cell carcinoma and oral precancerous conditions

Shah, Manisha H.; Sainger, Rachana; Telang, S.D.; Pancholi, G H; Shukla, Shailaja; Patel, Prabhudas S.

doi:10.4149/neo_2009_01_40

Cited by 16 publications

(14 citation statements)

References 40 publications

(55 reference statements)

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“…The data were consistent with our earlier studies which earlier have reported positive correlation of 97 kDa truncated E-cadherin protein with advanced stage and lymph node metastasis (Shah et al, 2009). Earlier studies have documented E-cadherin in non-tumor epithelium adjacent to oral cancer as a risk marker for the development of multiple tumors (Zhou et al, 2015).…”

Section: Discussionsupporting

confidence: 83%

Correlation between Loss of E-cadherin, Matrix-metalloproteinases and c-Jun expression in Oral Carcinogenesis

Vajaria¹,

Patel²,

Begum³

et al. 2017

AJOM

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Background: Earlier invitro studies have observed that loss of E-cadherin is responsible for progression and metastasis of cancer by upregulation of c-Jun protein. There being lack of simultaneous evaluation of matrix metalloproteinase (MMP) -2 and -9, E-cadherin and c-Jun mRNA and protein.Objective: This study aimed to correlate the above-mentioned parameters to evaluate the pathway of oral carcinogenesis. Methods:The study included 100 controls, 50 patients with oral precancerous conditions (OPC) and 100 oral cancer patients. MMPs were evaluated by gelatin zymography, ECAD and CJUN mRNA and protein expression by semi quantitative RT-PCR and western blot respectively. Results:The levels of active and total MMP-2 and MMP-9 were significantly higher in patients with OPC and oral cancer patients as compared to controls. A significant increase in truncated E-cadherin and c-Jun protein was observed in malignant tissues as compared to adjacent normal tissues while CJUN mRNA levels were comparable. Higher values of c-Jun protein and MMPs, and lower values of ECAD mRNA were associated with reduced overall survival. A positive correlation was observed between truncated E-cadherin, MMPs and c-Jun protein. Conclusions:MMPs modulate cell-cell adhesion by increasing truncation of E-cadherin resulting in loss of Ecadherin which is responsible for upregulation of c-Jun protein in oral cancer.

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Section: Discussionsupporting

confidence: 83%

Correlation between Loss of E-cadherin, Matrix-metalloproteinases and c-Jun expression in Oral Carcinogenesis

Vajaria¹,

Patel²,

Begum³

et al. 2017

AJOM

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“…Furthermore, the reduction in E-cadherin expression with increasing severity of histopathological dysplasia grading was also observed. Previous studies have found E-cadherin expression to be significantly reduced in dysplastic oral mucosa and OCSCC [ 8 , 15 , 17 , 18 ], considering that loss of cohesion is one of the key features of dysplasia. Also recently published data by Freitas Silva et al [ 21 ] reinforced our findings by demonstrating E-cadherin downregulation leading to phenotypic changes in early stages of oral carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

E-cadherin as a potential biomarker of malignant transformation in oral leukoplakia: a retrospective cohort study

et al. 2014

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BackgroundNumerous attempts have been made to establish and develop tumor markers that could determine the susceptibility of normal tissues to transform into cancerous ones. To determine whether altered expression patterns of E-cadherin could be an early event in the progression of potentially malignant disorders to oral squamous cell carcinoma, this study aimed to assess the relationship between the immunoexpression of E-cadherin and the different degrees of epithelial dysplasia in oral leukoplakia.MethodsSurgically excised specimens from patients with oral leukoplakia (n = 31), oral cavity squamous cell carcinoma with cervical lymph node metastasis (n = 12) and normal oral mucosa (n = 9) were immunostained for E-cadherin. Oral leukoplakia samples were distributed into low and high risk group according to a binary system for grading oral epithelial dysplasia. Comparative analyses between E-cadherin expression and microscopic features (WHO histological grading and epithelial dysplasia) were performed by Pearson Chi-square test (P < 0.05).ResultsDifferences in E-cadherin expression were observed between normal oral mucosa and low risk oral leukoplakia (P = 0.006), low and high risk oral leukoplakia (P = 0.019), and high risk oral leukoplakia and oral cavity squamous cell carcinoma with cervical lymph node metastasis (P = 0.0001). In addition, as epithelia undergo dysplastic changes, the risk of malignant transformation increases, and there is a reduction or loss of E-cadherin expression by keratinocytes. Reduced E-cadherin expression was an early phenomenon and it was observed in moderate-severe dysplasia, showing that the loss of epithelial cohesion may be an indicator of progression to oral cavity squamous cell carcinoma.ConclusionsE-cadherin could be used as a novel biomarker to identify lesions with potential risk for malignant transformation, which may provide opportunities for prophylactic interventions in high risk patient groups.

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“…33-37 The highly tumorigenic properties of the CSC suggest that they may be the critical population of cancer cells in the development of metastasis, just as they have been proven to be in primary tumor development and growth. 22 Clinically, CSC enrichment is directly linked to tumor recurrence, treatment failure, and metastases in HNSCC (reviewed in 14 ). The role of CSC in the development of metastasis is not yet well understood.…”

Section: Discussionmentioning

confidence: 99%

In vitro Evaluation of Sialyl Lewis X Relationship with Head and Neck Cancer Stem Cells

Czerwinski

Desiderio

Shkeir

et al. 2013

Otolaryngol.--head neck surg.

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Objective To evaluate in vitro the potential links between sialyl Lewis X (sLeX) and cancer stem cells (CSC) in head and neck squamous cell carcinoma (HNSCC). HNSCC is an aggressive malignancy with high mortality mainly due to metastasis. CSC have emerged as important players in HNSCC metastasis. sLeX is a tetrasaccharide carbohydrate known to play a key-role in metastatic dissemination by promoting binding of the tumor cells to the endothelium. Study Design Experimental, in vitro. Setting Laboratory of Head and Neck Cancer Metastasis, University of Michigan. Subjects and Methods A panel of stage- and anatomic-site specific primary and metastatic HNSCC cell lines was assessed by flow cytometry to quantify sLeX relative expression levels. Serum-free conditioned media from the same HNSCC lines was collected over a time-course of 72 hours and assessed by Western-blot for secreted sLeX expression. Representative HNSCC cell lines were cultured as floating orospheres (condition that enhance CSC growth) or under normal adherent conditions and characterized by flow cytometry for CSC markers (CD44, aldehyde dehydrogenase [ALDH]) comparatively with sLeX expression. Results sLeX is predominantly expressed in carcinomas originating from the oral cavity. Secreted sLeX is also found to be high in oral carcinomas and increased over the analyzed time course. Floating orospheres were strongly positive for CD44 and ALDH confirming CSC enrichment of the orospheres. Tumor cells grown as orospheres are 95-100% positive for sLeX compared to 10-40% of adherent counterpart. Conclusion These studies provide the first evidence of sLeX relationship with CSC in HNSCC.

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E-Cadherin truncation and Sialyl Lewis-X overexpression in oral squamous cell carcinoma and oral precancerous conditions

Cited by 16 publications

References 40 publications

Correlation between Loss of E-cadherin, Matrix-metalloproteinases and c-Jun expression in Oral Carcinogenesis

Correlation between Loss of E-cadherin, Matrix-metalloproteinases and c-Jun expression in Oral Carcinogenesis

E-cadherin as a potential biomarker of malignant transformation in oral leukoplakia: a retrospective cohort study

In vitro Evaluation of Sialyl Lewis X Relationship with Head and Neck Cancer Stem Cells

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