Downregulation and abnormal expression of E-cadherin and β-catenin in nasopharyngeal carcinoma: Close association with advanced disease stage and lymph node metastasis

Zheng, Zhong; Pan, Jie; Chu, B. W.-K.; Wong, Ying; Cheung, Any; Tsao, Sai‐Wah

doi:10.1016/s0046-8177(99)90123-5

Cited by 129 publications

(95 citation statements)

References 11 publications

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“…29 EBV microRNAs may also influence metastasis by targeting cell adhesion genes such as E-cadherin, 52 a frequently down-regulated gene in metastatic NPC. 53 Although we were unable to derive both RNA and protein from our NPC cases because of small biopsy samples, previous studies demonstrated only modestly inhibited protein production, rarely finding >4-fold reduction in protein levels. [54][55][56] Consistent with our Q-PCR and Western blot using EBV microRNA-transfected cell lines (Fig.…”

Section: Discussionmentioning

confidence: 81%

Profiling of Epstein‐Barr virus‐encoded microRNAs in nasopharyngeal carcinoma reveals potential biomarkers and oncomirs

Wong

Kong

Tsang

et al. 2011

Cancer

140

131

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BACKGROUND: Epstein-Barr virus (EBV) microRNAs are abundant in nasopharyngeal carcinoma (NPC) tumors. With recent advances in serum microRNA detection, the distinct presence of EBV microRNAs in serum could aid in screening endemic regions for NPC. A proposed network of genes targeted by these microRNAs could also shed light on EBV-associated tumorigenesis. METHODS: MicroRNA microarray profiling of 5 paired NPC biopsies was followed by validation of 12 up-regulated EBV microRNAs (BART1-3p, 2-5p, 5, 6-5p, 6-3p, 7, 8, 9, 14, 17-5p, 18-5p, 19-3p) in 15 additional cases by real-time polymerase chain reaction. Tumor (cellular) and serum microRNA copy numbers from the same 15 patients were correlated. Expression of the same microRNAs were also examined in EBV-positive cell lines C666 and NP460hTERTþEBV. Bioinformatic tools helped predict cellular target genes, which were later confirmed by gene expression analysis. RESULTS: The authors' high-throughput approach shows that EBV microRNAs are generally more up-regulated than microRNAs of human origin. Twenty-nine of 39 EBV microRNAs were significantly up-regulated in tumor versus their nontumor biopsies (P < .05). Upon successfully validating 12 selected EBV microRNAs in 15 additional paired NPC cases, the authors found that their distinct presence in the serum of NPC patients positively correlated with cellular copy numbers of EBV microRNAs. Further investigation of potential EBV microRNA target genes revealed inhibition of tumor suppressor genes (eg, PTEN) and extensive deregulation of several pathways frequently involved in NPC (eg, Wnt signaling). CONCLUSIONS: Increasing knowledge of host-virus interaction via microRNAs may provide feasible explanations underlying NPC tumorigenesis along with the development of biomarkers for screening high-risk populations. Cancer 2012;118:698-

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Section: Discussionmentioning

confidence: 81%

Profiling of Epstein‐Barr virus‐encoded microRNAs in nasopharyngeal carcinoma reveals potential biomarkers and oncomirs

Wong

Kong

Tsang

et al. 2011

Cancer

140

131

View full text Add to dashboard Cite

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“…E-cadherin is the major cadherin expressed on the surface of normal epithelial cells (37). E-cadherin expression is reduced during tumor progression and metastasis, and associated with poor prognosis in a variety of cancers (38)(39)(40). Based on these data, analysis of methylation status of E-cadherin gene promoter would be of great importance to understand the implication of this gene silencing in cervical cancer development.…”

Section: Discussionmentioning

confidence: 99%

Status of p16<SUP>INK4a</SUP> and E-Cadherin Gene Promoter Methylation in Moroccan Patients With Cervical Carcinoma

Attaleb¹,

W²,

Khyatti³

et al. 2009

oncol res

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Aberrant methylation of tumor suppressor gene promoters has been extensively investigated in cervical cancer. Transcriptional silencing, as a main consequence of hypermethylation of CpG islands, is the predominant mechanism of p16 INK4a and E-cadherin gene inactivation in malignant epithelial tumors. This study was conducted to evaluate the promoter methylation status of p16 INK4a and E-cadherin genes in 22 specimens of cervical carcinomas, four cervical cancer cell lines (HeLa, SiHa, Caski, C33A), and 20 human papillomavirus negative specimens, obtained from normal cervical swabs, using the methylation-specific PCR approach. Hypermethylation of the 5′ CpG island of the p16 INK4a and E-cadherin genes were found in 13 (59.1%) and 10 (45.5%) of 22 cervical cancer samples, respectively. Furthermore, our findings did not show any correlation between promoter methylation of p16 INK4a and E-cadherin genes and clinicopathological parameters, including HPV infection, phenotypic distribution, and stage of the disease. However, hypermethylation of E-cadherin gene promoter appears to be age related in cervical cancer, whereas the frequency of aberrant methylation of p16 INK4a gene promoter is unchanged according to the age of patients. Thus, caution must be made to use these markers in the diagnosis of cervical cancer. However, dietary or pharmaceutical agents that can inhibit these epigenetic events may prevent or delay the development of cervical cancer.

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“…[9][10][11][12] Several studies of epithelial malignancies have shown that E-cadherin or b-catenin can have a transcriptional and regulatory role in invasion and metastasis and is associated with a poor outcome. [13][14][15][16][17][18][19][20][21][22][23] E-cadherin is a 120 kDa calcium-dependent transmembrane glycoprotein encoded by the CDH1 gene located on chromosome 16q21, and it is expressed in most epithelial cells. 18 E-cadherin has a major role in establishing cell polarity and in maintaining normal tissue architecture.…”

mentioning

confidence: 99%

Upregulation of vimentin and aberrant expression of E-cadherin/β-catenin complex in oral squamous cell carcinomas: correlation with the clinicopathological features and patient outcome

et al. 2010

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Oral squamous cell carcinoma is a challenging oncology problem. A reliable biomarker for metastasis or high-risk prognosis in oral cancer patients remains undefined. Using quantitative immunohistochemistry, we examined the expression of vimentin, E-cadherin, and b-catenin in 83 oral squamous cell carcinoma patients, and the relationships between the expression of these markers and specific clinicopathological features were analysed. The high expression of vimentin was observed in 23 of 43 (53%) tumours from patients who eventually developed a recurrent tumour and was associated with recurrence and death (Po0.001 and o0.001, respectively). The decreased expression of E-cadherin was observed in 36 of 43 (84%) tumours from patients who eventually developed a recurrent tumour and was also associated with recurrence and death (Po0.001 and o0.001, respectively). Although no correlation between b-catenin expression in whole-tumour sections and clinicopathological features was observed, decreased b-catenin expression at the tumour invasive front was closely associated with recurrence and death (P ¼ 0.002 and 0.002, respectively). The expression of vimentin and that of E-cadherin were associated with survival and were independent prognostic factors in univariate and multivariate analyses. Our data show that the overexpression of vimentin was closely associated with recurrence and death in oral squamous cell carcinoma patients. The combination of the upregulation of vimentin and aberrant expression of E-cadherin/b-catenin complexes at the tumour invasive front may provide a useful prognostic marker in oral squamous cell carcinoma. Modern Pathology (2010) 23, 213-224; doi:10.1038/modpathol.2009 published online 13 November 2009 Keywords: vimentin; oral squamous cell carcinoma; immunohistochemistry Oral cancer is the sixth most frequently occurring cancer worldwide, accounting for 3-5% of all malignancies in both sexes.1,2 Over 90% of all oral carcinomas are classified as oral squamous cell carcinoma, which remains a challenging oncology problem.3 Although early-stage oral squamous cell carcinoma can be treated or cured, the prognosis for advanced oral squamous cell carcinoma (stage III and IV) is poor. The treatment of oral squamous cell carcinoma is usually based on surgery or radiation, with or without concomitant chemotherapy. Despite these advanced therapeutic strategies, the 5-year survival rate of oral squamous cell carcinoma (B50%) has not increased over the past four decades.3-5 Local or regional relapse and cervical lymph node metastasis are the most prevalent

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Downregulation and abnormal expression of E-cadherin and β-catenin in nasopharyngeal carcinoma: Close association with advanced disease stage and lymph node metastasis

Cited by 129 publications

References 11 publications

Profiling of Epstein‐Barr virus‐encoded microRNAs in nasopharyngeal carcinoma reveals potential biomarkers and oncomirs

Profiling of Epstein‐Barr virus‐encoded microRNAs in nasopharyngeal carcinoma reveals potential biomarkers and oncomirs

Status of p16<SUP>INK4a</SUP> and E-Cadherin Gene Promoter Methylation in Moroccan Patients With Cervical Carcinoma

Upregulation of vimentin and aberrant expression of E-cadherin/β-catenin complex in oral squamous cell carcinomas: correlation with the clinicopathological features and patient outcome

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