Association of E‐cadherin methylation with risk of nasopharyngeal cancer: A meta‐analysis

Wu, Cheng; Peng, Shan; Sun, Wei; Luo, Min; Su, Beibei; Liu, Dongbo; Hu, Guoqing

doi:10.1002/hed.25319

Cited by 7 publications

(4 citation statements)

References 41 publications

(82 reference statements)

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“…The cell migration capacity was clearly enhanced in HONE1-EBV cells. Meanwhile, expression of E-cadherin, an epithelial adhesion molecule, which frequently down-regulated in multiple malignancies, decreased 29. Furthermore, apoptosis was inhibited, and the anti apoptotic protein Bcl-2 was up-regulated in the HONE1-EBV cells.…”

Section: Discussionmentioning

confidence: 99%

<p>F factor plasmid-mediated Epstein-Barr virus genome introduction establishes an EBV positive NPC cell model</p>

Duan

Yang

et al. 2019

CMAR

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Background Most Epstein-Barr virus (EBV)-positive cells lose the EBV episomes upon prolonged propagation. Purpose The purposes of this study were to establish a simple cell model for nasopharyngeal carcinoma (NPC) research by introducing a plasmid with the EBV genome into NPC cells and then to investigate the resulting changes in malignant biological behaviour and NPC-associated signalling pathways. Methods HONE1 NPC cells were transfected with F-factor plasmids including the EBV genome (HONE1-EBV cells). Then cell proliferation, migration, cell cycle distribution and apoptosis were evaluated in vitro by using CCK8, transwell and flow cytometry assays respectively. EBV-encoded proteins and cell signal tranducting proteins were detected by western blot assays. EBV-encoded RNAs were detected by in situ hybridization. EBV particles were assayed by transmission electron microscope (TEM). The morphology of cells were detected by immunofluorescence assays for alpha-tubulin. Results Latent membrane protein 1 (LMP1), latent membrane protein 2A (LMP2A), Epstein-Barr nuclear antigen 1 (EBNA1) and EBV-encoded small RNAs (EBERs) were successfully expressed in HONE1-EBV cells. No EBV particles were founded by TEM. Introduction of the EBV genome significantly promoted proliferation, cell cycle progression and migration and inhibited apoptosis in HONE1 cells. Immunofluorescence assays showed that the morphology of HONE1-EBV cells changed into spindle. Furthermore, EBV genome introduction significantly inhibited the JAK/STAT signalling pathway, while it activated the PI3K-AKT and NF-κB signalling pathways in HONE1 cells. Conclusion These findings suggest that F-factor plasmid-mediated EBV genome introduction was successful in constructing an EBV positive cell model, which showed deteriorated biological behavior and activated NPC-associated signalling pathways. This model can serve as a good tool for studying EBV in NPC, but the subtle differences in cancer-associated pathways must be considered.

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Section: Discussionmentioning

confidence: 99%

<p>F factor plasmid-mediated Epstein-Barr virus genome introduction establishes an EBV positive NPC cell model</p>

Duan

Yang

et al. 2019

CMAR

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“… 26 , 27 Decreased or absent expression of E-cadherin can lead to weakened adhesion between cancer cells, which in turn makes cancer cells prone to shedding and metastasis, and promotes tumorigenesis, invasion and metastasis of epithelial tumors (including NPC). 28 , 29 Knockdown of the long non-coding RNA MALAT1 (Metastasis-Associated Lung Adenocarcinoma Transcription-1) inhibits proliferation, invasion, and EMT of NPC cells, as shown by increased expression of E-cadherin and decreased expression of N-cadherin. 30 …”

Section: Discussionmentioning

confidence: 99%

Hsa_circ_0013561 promotes progression of nasopharyngeal carcinoma by activating JAK2/STAT3 signaling pathway

Kaisai,

Mantang,

Tailei

et al. 2024

Brazilian Journal of Otorhinolaryngology

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“…Furthermore, ZNF667-AS1 could strikingly increase the expression of E-cadherin. As an epithelial marker, E-cadherin was inactivated in many kinds of cancers, and its inactivation was partly attributed to the aberrant promoter CpG sites hypermethylation 29,30 . The methylation of cytosine was for a long time assumed to be permanent, but the discovery of the ability of the TET enzymes to convert 5mC to 5hmC, and further to 5fC and 5caC has suggested a new mechanism by which DNA can be demethylated.…”

Section: Discussionmentioning

confidence: 99%

Aberrant hypermethylation-mediated downregulation of antisense lncRNA ZNF667-AS1 and its sense gene ZNF667 correlate with progression and prognosis of esophageal squamous cell carcinoma

Zhao

et al. 2019

Cell Death Dis

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Natural antisense lncRNAs can interfere with their corresponding sense transcript to elicit concordant or discordant regulation. LncRNA ZNF667-AS1 and its sense gene ZNF667 were found to be downregulated in esophageal squamous cell carcinoma (ESCC) tissues by RNA sequencing; however, the exact roles of both genes in ESCC occurrence and development have not been clarified. This study was to investigate the expression patterns, epigenetic inactivation mechanisms, function, and prognostic significance of ZNF667-AS1 and ZNF667 in ESCC tumorigenesis. Frequent downregulation of ZNF667-AS1 and ZNF667 was detected in esophageal cancer cells and ESCC tissues. The expression levels of ZNF667-AS1 and ZNF667 were significantly reversed by treatment with 5-Aza-dC and TSA in esophageal cancer cell lines. The CpG sites hypermethylation within proximal promoter influenced the binding ability of transcription factor E2F1 to the binding sites and then affected the transcription and expression of ZNF667-AS1 and ZNF667. Overexpression of ZNF667-AS1 and ZNF667 suppressed the viability, migration, and invasion of esophageal cancer cells in vitro. Overexpression of ZNF667-AS1 increased mRNA and protein expression level of ZNF667. ZNF667-AS1 interacts with and recruits TET1 to its target gene ZNF667 and E-cadherin to hydrolyze 5′-mc to 5′-hmc and further activates their expression, meanwhile, ZNF667-AS1 also interacts with UTX to decrease histone H3K27 tri-methylation to activate ZNF667 and E-cadherin expression. Furthermore, ZNF667-AS1 or ZNF667 expression and promoter methylation status were correlated with ESCC patients’ survival. Thus, these findings suggest that ZNF667-AS1 and ZNF667 may act as tumor suppressors and may serve as potential targets for antitumor therapy.

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Association of E‐cadherin methylation with risk of nasopharyngeal cancer: A meta‐analysis

Abstract: The E-cadherin methylation is strongly associated with the incidence of NPC, which can serve as an effective biomarker for early detection of NPC.

Cited by 7 publications

References 41 publications

<p>F factor plasmid-mediated Epstein-Barr virus genome introduction establishes an EBV positive NPC cell model</p>

<p>F factor plasmid-mediated Epstein-Barr virus genome introduction establishes an EBV positive NPC cell model</p>

Hsa_circ_0013561 promotes progression of nasopharyngeal carcinoma by activating JAK2/STAT3 signaling pathway

Aberrant hypermethylation-mediated downregulation of antisense lncRNA ZNF667-AS1 and its sense gene ZNF667 correlate with progression and prognosis of esophageal squamous cell carcinoma

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