Aberrant DNA methylation links cancer susceptibility locus 15q25.1 to apoptotic regulation and lung cancer.
Aberrant DNA methylation links cancer susceptibility locus 15q25.1 to apoptotic regulation and lung cancer.
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DOI:
10.1158/0008-5472.can-09-4550
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发表时间:
2010-04-01
期刊:
影响因子:
11.2
通讯作者:
Herceg Z
中科院分区:
文献类型:
--
作者:
Paliwal A;Vaissière T;Krais A;Cuenin C;Cros MP;Zaridze D;Moukeria A;Boffetta P;Hainaut P;Brennan P;Herceg Z
Nicotinic acetylcholine receptor (nAChR) genes form a highly conserved gene cluster at the lung cancer susceptibility locus 15q25.1. In this study, we show that the CHRN α 3 gene encoding nAChR α 3 subunit is a frequent target of aberrant DNA hypermethylation and silencing in lung cancer, whereas the adjacent CHRN β 4 and CHRN α 5 genes exhibit moderate and no methylation, respectively. Treatment of cancer cells exhibiting CHRN α 3 hypermethylation with DNA methylation inhibitors caused demethylation of the CHRN α 3 promoter and gene re-activation. Restoring CHRN α 3 levels through ectopic expression induced apoptotic cell death. shRNA-mediated depletion of nAChR α 3 in CHRN α 3-expressing lung cancer cells elicited a dramatic Ca2+ influx response in the presence of nicotine, followed by activation of the Akt survival pathway. CHRN α 3-depleted cells were resistant to apoptosis-inducing agents, underscoring the importance of epigenetic silencing of the CHRN α 3 gene in human cancer. In defining a mechanism of epigenetic control of nAChR expression in non-neuronal tissues, our findings offer a functional link between susceptibility locus 15q25.1 and lung cancer, and suggest nAChRs as theranostic targets for cancer detection and chemoprevention.