Optimization of comparative expressed sequence hybridization for genome-wide expression profiling at chromosome level

Ling, Zhi‐Qiang; Sugihara, Hiroyuki; Tatsuta, Takeshi; Mukaisho, Ken‐ichi; Hattori, Takanori

doi:10.1016/j.cancergencyto.2007.02.011

Cited by 6 publications

(10 citation statements)

References 22 publications

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“…These non-significant results may be due to the fact that human clinical samples are heterogeneous, with cytological diversity and different variants that may neutralize the aberrant expression of genes. Genes with transcriptional inactivation due to methylation are sensitive to DNA methylation inhibitors and can easily be reactivated (32). The methylation inhibitor 5-aza-dC, can be incorporated during DNA synthesis, and reduces the capacity for DNA methylation by DNMTs, thus reversing the methylation status of the promoters of genes (32,33).…”

Section: Discussionmentioning

confidence: 99%

“…Genes with transcriptional inactivation due to methylation are sensitive to DNA methylation inhibitors and can easily be reactivated (32). The methylation inhibitor 5-aza-dC, can be incorporated during DNA synthesis, and reduces the capacity for DNA methylation by DNMTs, thus reversing the methylation status of the promoters of genes (32,33). In the present study, methylated BCL cell lines (Raji, CTB-1, SLVL) and a primary patient cell line were treated with 5-aza-dC.…”

Section: Discussionmentioning

confidence: 99%

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Chromosome 16q genes CDH1, CDH13 and ADAMTS18 are correlated and frequently methylated in human lymphoma

et al. 2016

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Abstract. The products of the E-cadherin (CDH1), H-cadherin (CDH13) and a disintegrin and metalloproteinase with thrombospondin motif 18 (ADAMTS18) genes are proteins displaying structural features and functions on the cell surface membrane, and have been reported to be involved in cancer progression. Using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and methylation-specific PCR (MSP) analysis, the promoter methylation status and messenger RNA (mRNA) expression levels of CDH1, CDH13 and ADAMTS18, which are putative tumor-suppressor genes located on chromosome 16q, were evaluated. In addition, the mRNA expression levels of DNA methyltransferases (DNMTs) 1, 3A and 3B were examined, and the correlations among the different parameters analyzed were studied in 36 lymphomas and 16 non-malignant lymphoid tissue samples. A significant positive correlation was identified between the expression levels of CDH1 and CDH13 (r=0.735, P<0.01). ADAMTS18 expression also exhibited a significant positive correlation with both CDH1 and CDH13 mRNA expression levels (r=0. 625, P<0.01; and r=0.720, P<0.01, respectively). Our results indicated that CDH1, CDH13 and ADAMTS18, which are localized on chromosome 16q, are remarkably correlated and frequently methylated in human lymphomas, and their methylation could not be explained solely by the mRNA expression level of DNMTs.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chromosome 16q genes CDH1, CDH13 and ADAMTS18 are correlated and frequently methylated in human lymphoma

et al. 2016

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“…significant dNA modification mechanisms is cpG island methylation (33). cpG islands are c and G rich sequences and hypermethylation of cpG islands can inhibit or silence gene transcription, leading to a reduction or loss of functional protein and promote tumor development (33)(34)(35)(36). Methylation is the most common dNA modification and in some cases it is the only mechanism of inactivation of tumor suppressor genes (37).…”

Section: Discussionmentioning

confidence: 99%

“…Methylation is the most common dNA modification and in some cases it is the only mechanism of inactivation of tumor suppressor genes (37). Genes with transcriptional inactivation due to methylation are very sensitive to dNA methylation inhibitors and can easily be re-activated (36). The methylation inhibitor 5-Aza-cdR has been extensively studied.…”

Section: Discussionmentioning

confidence: 99%

“…At the same time, it can covalently bind to dNA methyltransferases (dNMTs) and inhibit their biological activity, reversing the methylation status of tumor suppressor gene promoters. Gene silencing caused by methylation, particularly in tumor suppressor genes, can therefore be reactivated, resulting in gene expression and effectively suppressing tumor development (36)(37)(38)(39). CDH1 encodes a transmembrane protein subtype in the cadherin family, composed of 723-748 amino acid residues with extracellular, transmembrane, and intracellular regions.…”

Section: Methylation Statusmentioning

confidence: 99%

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Hypermethylation-modulated down-regulation of CDH1 expression contributes to the progression of esophageal cancer

Ling

Li²,

Ge³

et al. 2011

Int J Mol Med

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Abstract. CDH1, a cell adhesion molecule, which plays a key role in maintaining the epithelial phenotype, is regarded as an invasion-suppressor gene in light of accumulating evidence from in vitro experiments and clinical observations. In an attempt to clarify the mechanism responsible for inactivation of this gene in carcinomas, we investigated the methylation status of the CDH1 gene 5'-cpG islands and its regulatory mechanism in the progression of esophageal squamous cell carcinoma. Real-time methylation-specific polymerase chain reaction (qMSP) and treatment with the demethylating agent 5-aza-2'-deoxycytidine (5-Aza-cdR) were conducted to analyze the methylation status at the CDH1 promoter region in the human esophageal carcinoma cell lines, Ec1 and Ec9706. A total of 235 invasive esophageal squamous cell carcinomas (EScc) at stages I-IV and their corresponding normal tissue samples, were included in an immunohistochemistry study and methylation analysis of CDH1. The results demonstrate that in Ec1 and Ec9706 cells, the CDH1 promoter is methylated and treatment with 5-Aza-cdR restored CDH1 expression. Enhanced CDH1 expression decreased cell migration, invasion ability and increased adhesion ability. decreased CDH1 expression was detected in 59.6% of EScc tissues, compared with their adjacent non-neoplastic epithelia, which had a close correlation with the primary tumor status, lymph node status, distant metatasis and clinicopathologic stage. Hypermethylation at the CDH1 promoter was detected in 97.9% of 140 cases of EScc with low CDH1 expression. The methylation of CDH1 promoters (P=0.929) was closely correlated with the lack of expression of their corresponding proteins. The cox regression model for survival analysis showed that increases in CDH1 methylation had a greater impact on the prognosis than tumor clinical stage. These findings suggest that CDH1 gene silencing by promoter hypermethylation and the resultant reduction of CDH1 expression may play an important role in the progression of EScc. CDH1 methylation was a significant predictor of survival in EScc patients after surgery.

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Hypermethylation-modulated Downregulation of RASSF1A Expression Is Associated with the Progression of Esophageal Cancer

Mao¹,

Li²,

Zheng³

et al. 2011

Archives of Medical Research

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Optimization of comparative expressed sequence hybridization for genome-wide expression profiling at chromosome level

Cited by 6 publications

References 22 publications

Chromosome 16q genes CDH1, CDH13 and ADAMTS18 are correlated and frequently methylated in human lymphoma

Chromosome 16q genes CDH1, CDH13 and ADAMTS18 are correlated and frequently methylated in human lymphoma

Hypermethylation-modulated down-regulation of CDH1 expression contributes to the progression of esophageal cancer

Hypermethylation-modulated Downregulation of RASSF1A Expression Is Associated with the Progression of Esophageal Cancer

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