Molecular Genetic and Epigenetic analysis of NCX2/SLC8A2 at 19q13.3 in Human Gliomas

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Fältnamn	Indikatorer	Metadata
000		03381naa a2200481 4500
001		oai:DiVA.org:uu-123034
003		SwePub
008		100422s2010 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
009		oai:prod.swepub.kib.ki.se:120214644
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1230342 URI
024	7	a https://doi.org/10.1111/j.1365-2990.2010.01070.x2 DOI
024	7	a http://kipublications.ki.se/Default.aspx?queryparsed=id:1202146442 URI
040		a (SwePub)uud (SwePub)ki
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Qu, Mingqiu Uppsala universitet,Neurologi4 aut
245	1 0	a Molecular Genetic and Epigenetic analysis of NCX2/SLC8A2 at 19q13.3 in Human Gliomas
264	1	b Wiley,c 2010
338		a print2 rdacarrier
520		a AimLoss of heterozygosity (LOH) at 19q13.3 is a common genetic change in human gliomas, indicating yet unknown glial-specific tumour suppressor genes in this chromosome region. NCX2/SLC8A2 located on chromosome 19q13.32 encodes a Na(+)/Ca(2+)exchanger, which contributes to intracellular Ca(2+)homeostasis. Its expression is restricted to brain, and it is neither present in other normal tissues nor in gliomas at any significant level. The aim of this study was to investigate if NCX2 might be a tumour suppressor gene involved in glioma.MethodsWe performed a systematic analysis of NCX2 in 42 human gliomas using microsatellite analysis for evaluation of LOH at 19q, DNA sequencing and DNA methylation analysis.ResultsExcept for three known intragenic SNPs, rs12459087, rs7259674, and rs8104926, no NCX2 sequence variations were detected in any of the tumour samples. Furthermore, a CpG island in the 5' promoter region of NCX2 was unmethylated. Interestingly, the CpG sites of three gene-body CpG islands located in exon 2, intron 2-3 and exon 3 and of a 5' CpG rich area relevant to so called CpG island shore of NCX2 were methylated in all 8 glioma samples and in 3 established glioma cell lines tested. Surprisingly, NCX2 could be activated by addition of the DNA methylation inhibitor 5-aza-2'-deoxycytidine to glioma cell lines in which NCX2 was completely silent.ConclusionResults indicate that DNA methylation may play a key role in the transcriptional silencing of NCX2.
653		a 19q13.3
653		a DNA methylation
653		a Glioma
653		a Mutation
653		a NCX2
653		a Single nucleotide polymorphism
653		a MEDICINE
653		a MEDICIN
653		a Neurology
653		a Neurologi
700	1	a Jiao, Hongu Karolinska Institutet4 aut
700	1	a Zhao, Jianu Karolinska Institutet4 aut
700	1	a Ren, Zhi-Pingu Uppsala universitet,Institutionen för genetik och patologi4 aut
700	1	a Smits, Anjau Uppsala universitet,Neurologi4 aut0 (Swepub:uu)anjasmit
700	1	a Kere, Juhau Karolinska Institutet4 aut
700	1	a Nistér, Monicau Karolinska Institutet4 aut
710	2	a Uppsala universitetb Neurologi4 org
773	0	t Neuropathology and Applied Neurobiologyd : Wileyg 36:3, s. 198-210q 36:3<198-210x 0305-1846x 1365-2990
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-123034
856	4 8	u https://doi.org/10.1111/j.1365-2990.2010.01070.x
856	4 8	u http://kipublications.ki.se/Default.aspx?queryparsed=id:120214644

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Av författaren/redakt...: Qu, Mingqi; Jiao, Hong; Zhao, Jian; Ren, Zhi-Ping; Smits, Anja; Kere, Juha; visa fler...; Nistér, Monica; visa färre...

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Av lärosätet: Uppsala universitet; Karolinska Institutet

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