DNA Methylation and Cancer Development: Molecular Mechanism

Akhavan‐Niaki, Haleh; Samadani, Ali Akbar

doi:10.1007/s12013-013-9555-2

Cited by 122 publications

(89 citation statements)

References 120 publications

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“…Gene methylation is a major source of epigenetic modification in mammals, and changes in methylation patterns play a key role in tumorigenesis in humans. Particularly, promoter CpG island methylation is related to inactivation and silencing, resulting in decreased expression of tumor suppressors, chromosome inactivation and affects the development of tumors (Baylin et al, 2005;Hesson et al, 2007;Akhavan-Niaki et al, 2013). Aberrant methylation within the promoter region of RASSF1A has been reported in various tumors, including NSCLC (Dammann et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Associations Between RASSF1A Promoter Methylation and NSCLC: A Meta-analysis of Published Data

Liu¹,

Tan²,

Guo³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Background: RASSF1A has been reported to be a candidate tumor suppressor in non-small cell lung cancer (NSCLC). However, the association between RASSF1A promoter methylation and NSCLC remains unclear, particularly in regarding links to clinicopathologic features. Methods: Eligible studies were identified through searching PubMed, EMBASE, Cochrane Library and China National Knowledge Infrastructure (CNKI) databases. Studies were pooled and odds ratios (ORs) with corresponding confidence intervals (CIs) were calculated. Funnel plots were also performed to evaluate publication bias. Keywords: RAS associations domain family protein 1A -non-small cell lung cancer -methylation -odds ratio

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Section: Discussionmentioning

confidence: 99%

Associations Between RASSF1A Promoter Methylation and NSCLC: A Meta-analysis of Published Data

Liu¹,

Tan²,

Guo³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…Generally, 70-80% CpG sites in the human genome are methylated (12). Abnormal DNA methylation is a common event in human cancers, including hypermethylation of a tumor suppressor gene, hypomethylation of an oncogene and global hypomethylation of the genome (13)(14)(15). DNA methylation is a reversible process, making it a promising target for cancer therapy.…”

Section: Introductionmentioning

confidence: 99%

The anti-tumor effects of Mfn2 in breast cancer are dependent on promoter DNA methylation, the P21Ras motif and PKA phosphorylation site

Dong

Shan

et al. 2018

Oncol Lett

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Abstract. Mitofusin 2 (Mfn2) is expressed in numerous human tissues and serves a pivotal role in cell proliferation. However, Mfn2 is considered as an anti-tumor gene, and is silenced in human malignant tumors, including those of breast cancer. However, the mechanisms contributing to Mfn2 silencing and the mechanism of its anti-tumor function in breast cancer remain unclear. In the present study, hypoexpression of Mfn2, and hypermethylation of its promoter, was confirmed in human breast cancer cells and in breast cancer tissues by reverse transcription-quantitative polymerase chain reaction (PCR) and methylation specific PCR, respectively. Chemical demethylation treatment with 5-aza-2'-deoxycytidine upregulated the mRNA expression level of Mfn2 in MCF-7 cells in a dose-dependent manner. In addition, overexpression of Mfn2 repressed the proliferation, migration and invasion of MCF-7 cells, mediated by inhibition of the Ras-extracellular signal-regulated kinase (ERK)1/2 signaling pathway. However, overexpression of Mfn2 with deletion of the p21Ras motif (Mfn2 ΔRas ) and protein kinase A (PKA) phosphorylation site (Mfn2 ΔPKA ) partially reduced the anti-tumor function of Mfn2, and inhibited the Ras-ERK1/2 signaling pathway. Taken together, the present study confirmed the anti-tumor effects of Mfn2 in human breast cancer and clarified that the mechanism of its anti-tumor functions includes promoter DNA methylation, the P21 Ras binding site and PKA phosphorylation.

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“…Aberrant promoter hypermethylation contributes to the transcriptional inactivation of a number of genes in various malignant diseases (1). However, the precise mechanisms underlying this aberration remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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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DNA Methylation and Cancer Development: Molecular Mechanism

Cited by 122 publications

References 120 publications

Associations Between RASSF1A Promoter Methylation and NSCLC: A Meta-analysis of Published Data

Associations Between RASSF1A Promoter Methylation and NSCLC: A Meta-analysis of Published Data

The anti-tumor effects of Mfn2 in breast cancer are dependent on promoter DNA methylation, the P21Ras motif and PKA phosphorylation site

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

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