Evidence map›Paper›PMID 20163738›Full record

ArticleBMC cancer2010

Methylation status of individual CpG sites within Alu elements in the human genome and Alu hypomethylation in gastric carcinomas.

Shengyan Xiang, Zhaojun Liu, Baozhen Zhang, Jing Zhou, Bu-Dong Zhu, Jiafu Ji, Dajun Deng

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 17% of its field
1 · What the graph read from it

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3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 40 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Shengyan XiangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Beijing Cancer Hospital and Institute, Peking University School of Oncology, Haidian District, Beijing, 100142, China.
Zhaojun Liu
Baozhen Zhang
Jing Zhou
Bu-Dong Zhu
Jiafu Ji
Dajun Deng
Peking University · CNPeking University Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlu methylation is correlated with the overall level of DNA methylation and recombination activity of the genome. However, the maintenance and methylation status of each CpG site within Alu elements (Alu) and its methylation status have not well characterized. This information is useful for understanding natural status of Alu in the genome and helpful for developing an optimal assay to quantify Alu hypomethylation.

methodsBisulfite clone sequencing was carried out in 14 human gastric samples initially. A Cac8I COBRA-DHPLC assay was developed to detect methylated-Alu proportion in cell lines and 48 paired gastric carcinomas and 55 gastritis samples. DHPLC data were statistically interpreted using SPSS version 16.0.

resultsFrom the results of 427 Alu bisulfite clone sequences, we found that only 27.2% of CpG sites within Alu elements were preserved (4.6 of 17 analyzed CpGs, A approximately Q) and that 86.6% of remaining-CpGs were methylated. Deamination was the main reason for low preservation of methylation targets. A high correlation coefficient of methylation was observed between Alu clones and CpG site J (0.963), A (0.950), H (0.946), D (0.945). Comethylation of the sites H and J were used as an indicator of the proportion of methylated-Alu in a Cac8I COBRA-DHPLC assay. Validation studies showed that hypermethylation or hypomethylation of Alu elements in human cell lines could be detected sensitively by the assay after treatment with 5-aza-dC and M.SssI, respectively. The proportion of methylated-Alu copies in gastric carcinomas (3.01%) was significantly lower than that in the corresponding normal samples (3.19%) and gastritis biopsies (3.23%).

conclusionsMost Alu CpG sites are deaminated in the genome. 27% of Alu CpG sites represented in our amplification products. 87% of the remaining CpG sites are methylated. Alu hypomethylation in primary gastric carcinomas could be detected with the Cac8I COBRA-DHPLC assay quantitatively.

Indexed as

Alu ElementsDNA MethylationAdultAgedAged, 80 and overCell Line, TumorChromatography, High Pressure LiquidCpG IslandsDNA Mutational AnalysisFemaleGenome, HumanHumansMaleMiddle AgedStomach Neoplasms

Identifiers

PMID20163738
PMCPMC2834620
OpenAlexW1981637597

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.