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Background  MicroRNA (miR)  miR - 34 a, - 34b/c , - 124-1  and - 203  are tumor suppressor miRs implicated in carcinogenesis.    Methods  We studied DNA methylation of these miRs in Philadelphia-negative (Ph-ve) myeloproliferative neoplasms (MPNs). Methylation-specific PCR (MSP), verified by direct sequencing of the methylated MSP products, was performed in cell lines, normal controls and diagnostic marrow samples of patients with MPNs.    Results  Methylation of these miRs was absent in the normal controls.  miR-34b/c  were homozygously methylated in HEL cells but heterozygously in MEG-01. In HEL cells, homozygous  miR-34b/c  methylation was associated with miR silencing, and 5-aza-2'-deoxycytidine treatment led to re-expression of both  miR-34b  and  miR-34c , consistent with that both miRs are under the regulation of the same promoter CpG island.  miR-34a  was heterozygously methylated in MEG-01 and K-562.  miR-203  was completely unmethylated in K-562 and SET-2 but no MSP amplification was found in both HEL and MEG-01, suggestive of miR deletion. In primary samples, four each had  miR-34b/c  and  -203  methylation, in which two had concomitant methylation of  miR-34b/c  and  -203 .  miR-34a  was methylated in one patient and none had methylation of  miR-124-1 . Seven patients (15.6%) had methylation of at least one of the four miRs. miR methylation did not correlate with clinical parameters, disease complications or JAK2 V617F mutation.    Conclusion  This is the first report of miR hypermethylation in MPNs.  miR-203  hypermethylation is not specific to Ph+ve leukemias but also present in Ph-ve MPNs.  miR-34b/c  methylation was associated with reversible miR silencing. There was no correlation of miR methylation with clinical demographic data or outcome.

Methylation of miR-34a, miR-34b/c, miR-124-1 and miR-203 in Ph-negative myeloproliferative neoplasms