The Levels of H11/HspB8 DNA methylation in human melanoma tissues and xenografts are a critical molecular marker for 5-Aza-2'-deoxycytidine therapy.
The Levels of H11/HspB8 DNA methylation in human melanoma tissues and xenografts are a critical molecular marker for 5-Aza-2'-deoxycytidine therapy.
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DOI：
10.3109/07357907.2011.584588
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发表时间：
2011-07
影响因子：
2.4
通讯作者：
Aurelian L
中科院分区：
文献类型：
--
作者：
Smith CC;Li B;Liu J;Lee KS;Aurelian L
H11/HspB8是一种功能独特的小热休克蛋白。在27/35（77%）的黑色素瘤组织/早期培养中，它通过DNA甲基化导致黑素细胞生长停滞，与细胞周期蛋白E/cdk2和-catenin转录活性位点Ser552的磷酸化抑制有关。5'- aza -2-脱氧胞苷（Aza-C）诱导黑色素瘤细胞死亡与H11/HspB8 DNA甲基化水平相关（p<0.001）。在低/中度H11/HspB8甲基化的细胞系中，PI3-K抑制增加了aza - c诱导的细胞死亡。Aza-C抑制与H11/HspB8甲基化水平相关的黑色素瘤异种移植物的生长，非甲基化/非tak1结合的H11/HspB8突变体赋予Aza-C抗性。H11/HspB8是去甲基化治疗的潜在分子标记。
H11/HspB8 is a functionally distinct small heat shock protein. It causes growth arrest in melanocytes, associated with inhibition of cyclin E/cdk2 and -catenin phosphorylation at the transcriptional activity site Ser552 and is silenced through DNA methylation in 27/35 (77%) melanoma tissues/early cultures. 5'-Aza-2-deoxycytidine (Aza-C) induces melanoma cell death correlated with the levels of H11/HspB8 DNA methylation (p<0.001). In lines with low/moderate H11/HspB8 methylation, PI3-K inhibition increases Aza-C-induced cell death. Aza-C Inhibits growth of melanoma xenografts related to the levels of H11/HspB8 methylation, and a non-methylated/non-TAK1 binding H11/HspB8 mutant confers Aza-C resistance. H11/HspB8 is a potential molecular marker for demethylation therapies.
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