• Environmental Analysis Health and Toxicology
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• v.22 no.2 s.57
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• pp.137-145
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• 2007

The effect of cadmium chloride $(CdCl_2)$ on the expression of E-cadherin was examined in bEnd.3 mouse brain endothelial cells. $CdCl_2$ induced $PGE_2$ release, which were blocked by non-steroidal antinflamatory drugs (NSAIDs) such as indomethacin and NS398 indicating the expression of COX-2 might contribute to $PGE_2$ production. $CdCl_2$ decreased the expression of E-cadherin, but not VE-cadherin at levels of mRNA and protein. Reduced expression level of E-cadherin was restored by NSAIDs, which was reversed by the addition of $PGE_2$. $CdC_2$-induced decrease of E-cadherin level was also recovered by antioxidants including N-acetylcyteine (NAC) and trolox. Together with previous report which showed $CdCl_2$ induced COX-2 expression in a cellular oxidative stress dependent manner, these data suggest that $CdCl_2$ decreases E-cadherin expression through induction of cellular oxidative stress and in turn COX-2 expression in brain endothelial cells.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.20
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• pp.8847-8853
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• 2014

The aim of this study was to establish the expression and localization of E-cadherin and ${\beta}$-catenin in oral squamous cell carcinomas (OSCC) so that we could correlate the findings with prognostic-relevant histopathological variables. E-cadherin and ${\beta}$-catenin expression in normal oral epithelia and in oral squamous cell carcinomas was examined immunohistochemically, and associations with histopathological differentiation and prognosis were then analyzed in 33 patients who had been operated on for OSCC. E-cadherin expression was found in (82%) of the squamous cells of well differentiated OSCC, (61%) of moderately differentiated and (39%) of poorly differentiated. E-cadherin expression was significantly associated with histological grade (p=0.000). No nuclear staining was detected. In (19.5%) of the cells E-cadherin localized in the cytoplasm, with no correlation to the histological grade (p=0.106). ${\beta}$-Catenin expression was found in 87% of the squamous cells of well differentiated OSCC, 67% of moderately differentiated and 43% of poorly differentiated, the expression was significantly associated with histological grade (p=0.000). the nuclear ${\beta}$-Catenin expression appeared in 3.3% of the cells and it was correlated to the histological grade (p=0.000). In (23.5%) of the cells ${\beta}$-Catenin localized in the cytoplasm, with correlation to the histological grade (p=0.002). According to this study the expression of ${\beta}$-catenin and E-cadherin were independent prognostic factors for histological grade. E-cadherin was closely linked to ${\beta}$-catenin expression in OSCC (p=0.000) and to tumor differentiation. That reflects a structural association and the role of both in tumor progression.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.5
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• pp.2145-2152
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• 2014

Background: The survival rate for oral squamous cell carcinoma (OSCC) has remained generally unchanged in the past three decades, underlining the need for more biomarkers to be developed to aid prognostication and effective management. The prognostic potential of E-cadherin expression in OSCCs has been variable in previous studies while galectin-9 expression has been correlated with improved prognosis in other cancers. The aim of the present study was to investigate the expression of galectin-9 and E-cadherin in OSCC and their potential as prognostic biomarkers. Materials and Methods: E-cadherin and Galectin-9 expression was examined by immunohistochemistry in 32 cases of OSCC of the buccal mucosa (13 with and 19 without lymph node metastasis), as well as 6 samples of reactive lesions and 5 of normal buccal mucosa. Results: The expression of E-cadherin in OSCC was significantly lower than the control tissues but galectin-9 expression was conversely higher. Median E-cadherin HSCOREs between OSCCs positive and negative for nodal metastasis were not significantly different. Mean HSCOREs for galectin-9 in OSCC without lymph node metastasis ($127.7{\pm}81.8$) was higher than OSCC with lymph node metastasis ($97.9{\pm}62.9$) but this difference was not statistically significant. Conclusions: E-cadherin expression is reduced whilst galectin-9 expression is increased in OSCC. However, the present results suggest that E-cadherin and galectin-9 expression may not be useful as prognostic markers for OSCC.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.2
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• pp.669-672
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• 2013

Objective: To investigate the expression of Twist and E-cadherin in ovarian cancer tissues as well as the role of epithelial-mesenchymal transformation (EMT) in ovarian cancer metastasis. Method: The expressions of Twist and E-cadherin in 54 cases of ovarian cancer and paracancerous tissues were detected by Western blottin g and reverse transcriptase polymerase chain reaction. We used RNA interference to silence Twist expression in human ovarian cancer cell line, and detected E-cadherin expression using Western blotting. Results: There was an increase in the relative abundance of Twist proteins and a decrease in E-cadherin in ovarian cancer compared with normal ovary tissues (P < 0.05). The expression levels of Twist and E-cadherin mRNA were $1.49{\pm}0.53$ and $0.82{\pm}0.24$ in ovarian cancer, and $1.14{\pm}0.38$ and $1.08{\pm}0.19$ in paracancerous tissues, respectively. The difference between the indicators in ovarian cancer and in paracancerous tissues was statistically significant (P < 0.05). When the Twist expression was silenced in an ovarian cancer cell line, the expression of the E-cadherin protein increased (P<0.05). Conclusion: The expression of Twist is upregulated, whereas that of E-cadherin is downregulated in ovarian cancer. EMT, mediated by Twist, may be correlated with ovarian cancer metastasis.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.36 no.6
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• pp.453-459
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• 2010

Introduction: Ameloblastic carcinoma is a rare malignant lesion, and may arise from either carcinoma ex-ameloblastoma or de novo carcinoma. Aberrant promoter hypermethylation of the tumor-associated genes leading to their inactivation is a common event in many cancer types. The p16/CDKN2/INK4A gene and p16 5 protein are involved directly in regulating the cell cycles. Cadherins are cell adhesion molecules that modulate the epithelial phenotype and regulate tumor invasion. The aim of this study was to evaluate the roles of p16 and E-cadherin methylation and loss of p16 and E-cadherin expression in the malignant transformation of an ameloblastoma. Materials and Methods: Eight cases of ameloblastoma, including 4 benign ameloblastomas without recurrence, 2 benign ameloblastomas with recurrence and 2 carcinoma ex-ameloblastomas, were examined. The promoter hypermethylation profile of the p16 and E-cadherin genes was studied using methylation-specific polymerase chain reaction (MSP) and immunohistochemical staining for p16 and E-cadherin expression. Results: 1) Aberrant CpG island methylation of the p16 gene was detected in 3 of the 4 benign ameloblastomas without recurrence and 1 of the 2 benign ameloblastomas with recurrence. 2) Aberrant CpG island methylation of the E-cadherin gene was found in 1 of the 4 benign ameloblastomas without recurrence. 3) A loss of p16 expression was noted in 1 of 4 benign ameloblastomas without recurrence and 1 of 2 carcinoma ex-ameloblastomas. 4) A loss of E-cadherin expression was noted in 2 of the 4 benign ameloblastomas without recurrence, 1 of the 2 benign ameloblastomas with recurrence and 2 of the 2 carcinoma ex-ameloblastomas. 5) A loss of p16 expression was observed in 1 of the 4 cases showing aberrant methylation of the p16 gene. 6) A loss of E-cadherin expression was observed in 3 benign ameloblastoma case showing aberrant methylation of the E-cadherin gene. Conclusion: These results suggest that loss of E-cadherin expression related to the other genetic pathway (not methylation) might be an adjuvant indicator predicting the malignant transformation of an ameloblastoma. However, the number of samples in this study was too small and the relationship between the treatment methods and clinical course were not defined. Therefore, further study will be needed.

• Korean Journal of Head & Neck Oncology
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• v.18 no.1
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• pp.23-29
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• 2002

Mutation of the P53 tumor suppressor gene playa major role in the development of many carcinomas, namely in the colon, breast and bladder, whereas the role played by such mutations in thyroid carcinogenesis remains controversial. Vascular endothelial growth factor (VEGF) induces proliferation of endothelial cells, stimulates angiogenesis, and increases vascular permeability. Increased VEGF expression has been associated with poor clinical outcomes in many malignancies E-cadherin, a calcium-dependent transmembrane glycoprotein, is an adhesion molecule Expression of p53, VEGF and E-cadherin was assessed immunohistochemically in 19 tall columnar variant of papillary carcinoma, 24 common papillary carcinoma and 7 follicular carcinoma. The aim of this study was to evaluate the expression of P53,VEGF and E-cadherin as a potential maker for the prognosis of thyroid carcinomas. The results are as follows: 1) There were no significance in any clinical parameters examined among tall columnar variant of papillary carcinoma, common papillary carcinoma and follicular carcinoma. 2) The expression of P53 demonstrated low in tall columnar variant of papillary carcinoma, common papillary carcinoma and follicular carcinoma, but a significantly high in regional lymph node metastasis. 3) The expression of VEGF demonstrated a significantly high in regional lymph node metastasis than those without metastasis in papillary thyroid carcinoma. 4) The expression of E-cadherin demonstrated less often among papillary carcinomas with lymph node metastasis than in those without metastasis in papillary thyroid carcinoma. In conclusion, it is suggested that VEGF and E-cadherin will be useful for the diagnosis of thyroid carcinoma and serves as a biological marker for thyroid carcinoma lymph node metastasis.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.2
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• pp.639-643
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• 2013

Aim: Connexin 43 (Cx43) and E-cadherin are important biomarkers related with cancer. Their expression at protein and mRNA levels was here investigated in 50 primary lung carcinoma tissues and 20 samples of adjacent normal tissue of Chinese patients with non-small cell lung cancer (NSCLC). Methods: Protein and mRNA expression were evaluated by ABC immunohistochemistry and RT-PCR. Results: (1) The positive expression rates of Cx43 and E-cadherin protein were higher in the adjacent normal tissues than those in the primary lung carcinoma tissues; (2) the positive expression rates of Cx43 and E-cadherin protein decreased with NSCLC progression; (3) the expression of E-cadherin protein was not related with the pathological type of NSCLC; and (4) the relative quantity of the Cx43 or E-cadherin mRNA expression was correlated with the the histological type, clinical stage, cancer cell differentiation and the lymph node metastasis. Conclusion: The data suggested that the Cx43 and E-cadherin are reduced with NSCLC progression, and might be important biomarkers for judging the metastasis and prognosis.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.28 no.5
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• pp.396-403
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• 2006

Changes in cell adhesion molecules are associated with infiltration and metastatic progression of cancer. Reduced expression of E-cadherin and ${\beta}-catenin$ complex in some carcinomas has been reported. The changes in the expression in oral squamous cell carcinoma (OSCC) is not fully understood and it also remains undetermined whether the expression of these adhesion molecules in metastatic lesions differs from that in the primary lesions. In the present study, therefore, we immunohistochemically examined the expression of E-cadherin and ${\beta}-catenin$ in 45 primary OSCCs and 19 metastatic lymph nodes. We compared the expression of these molecules between primary and metastatic lesions and investigated the correlation between the expression and clinicopathologic parameters. The expression of E-cadherin and ${\beta}-catenin$ was reduced in 35/45 (78.2%), 14/45 (31.2%) of primary tumors respectively, but 18/19 (94.7%) and 17/19 (89.4%) of lymph nodes showed preserved expression. The reduced expression of the E-cadherin was associated with lymph node metastasis, invasive mode and marginal status but no significant relationship was not found with ${\beta}-catenin$. In conclusion, the loss of E-cadherin and ${\beta}-catenin$ complex function is associated with progression of OSCC and suggest that the expression of this complex will be a supplementary prognostic tool.

• International Journal of Oral Biology
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• v.31 no.2
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• pp.27-32
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• 2006

Expression of invasion/metastasis suppressor, E-cadherin, is reduced in many types of human carcinomas. Although somatic and germline mutations in the CDH1, which encodes the human E-cadherin, have frequently been reported in cases with diffuse gastric and lobular breast cancers, irreversible genetic inactivations are rare in other human carcinomas. Recently, it has been well documented that some genes in human cancers may be inactivated by altered CpG methylation. Herein, we determined the expression and methylation status of E-cadherin in oral squamous cell carcinoma(SCC) by immunohistochemistry and methylation-specific PCR. The expression of E-cadherin was significantly higher in the well-differentiated oral SCCs than the moderately or poorly differentiated ones. None of eight tested benign epithelial hyperplasias showed aberrant methylation, whereas five of 12 oral squamous cell carcinomas showed aberrant methylation. When we compared E-cadherin expression with methylation status, oral SCCs with normal methylation showed a higher expression of E-cadherin than those with methylation. These findings suggest that aberrant CpG methylation of CDH1 promoter region is closely associated with transcriptional inactivation and might be involved in tumor progression of the oral mucosa.

• Journal of Gastric Cancer
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• v.8 no.2
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• pp.70-78
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• 2008

Purpose: VEGF-C and VEGF-D are angiogenetic factors, and abnormal expression of E-cadherin hasa role in the progression of gastric carcinoma. The aim of this study was to evaluate the relationship between the expression of E-cadherin, VEGF-C and VEGF-D with the presence of lymph node metastases (LNM) using cytokeratin 18 in early gastric cancer (EGC). Materials and Methods: Immunohistochemical staining for E-cadherin, VEGF-C and VEGF-D was performed in 49 EGC patients from March 1997 to December 2002. To evaluate the real extent of LNM, 1,562 lymph nodes from 49 patients were re-examined with the use of cytokeratin 18. Results: Eleven (0.7%) LNM were newly found in 12.2% (n=6) of patients. The real LNM rate was 3.6% in mucosal invasive (m) cancer and 38.1% in submucosal invasive (sm). Stage migration was seen in three patients (6.1%). Abnormal expression of E-cadherin was detected in 36.7% of the patients and expression of VEGF-C and VEGF-D was detected in 16.3% and 36.7% of the patients, respectively. Abnormal expression of E-cadherin was significantly correlated with tumor differentiation (P=0.0103) and Lauren classification (P<0.0001). There was no positive relationship of VEGF-C and VEGF-D expression with the clinicopathological findings for EGC including LNM. However, the frequency of lymph node metastases was significantly higher in patients that demonstrated abnormal expression of E-cadherin with positive immunoreactivity of VEGF-C or VEGF-D (P=0.031). Conclusion: In present study, we could not demonstrate a relationship between the presence of LNM and expression of VEGF-C and VEGF-D in EGC. However, VEGF-C or VEGF-D expression, in addition to the abnormal expression of E-cadherin, was correlated with the real extent of LNM in EGC.