Abstract
In the human placenta, DNA hypomethylation permits the expression of retrotransposon-derived genes that are normally silenced by methylation in somatic tissues. We previously identified hypomethylation of a retrotransposon-derived transcript of the voltage-gated potassium channel gene KCNH5 that is expressed only in human placenta. However, an RNA sequence from this placental-specific transcript has been reported in melanoma. This study examined the promoter methylation and expression of the retrotransposon-derived KCNH5 transcript in 25 melanoma cell lines to determine whether the acquisition of ‘placental’ epigenetic marks is a feature of melanoma. Methylation and gene expression analysis revealed hypomethylation of this retrotransposon in melanoma cell lines, particularly in those samples that express the placental KCNH5 transcript. Therefore we propose that hypomethylation of the placental-specific KCNH5 promoter is frequently associated with KCNH5 expression in melanoma cells. Our findings show that melanoma can develop hypomethylation of a retrotransposon-derived gene; a characteristic notably shared with the normal placenta.
Highlights
The human placenta, a globally hypomethylated tissue, is becoming increasingly known for harbouring unmethylated repetitive sequences [1]
The unique placental expression of these normally silenced repeat elements suggests a functional role for these sequences in the placenta, a role exemplified by the retrovirusderived gene syncytin (ERVWE1), which is essential for trophoblast differentiation during placental development [9,10]
The New Zealand melanoma (NZM) cell lines used in this study were generated from surgical samples of metastatic melanoma, obtained with written consent from all patients under the guidelines and specific approval of the Auckland Area Health Board Ethics Committee (New Zealand)
Summary
The human placenta, a globally hypomethylated tissue, is becoming increasingly known for harbouring unmethylated repetitive sequences [1]. The epigenetic activation of repeat sequences in the placenta is demonstrated by the finding that many repetitive elements that are normally silenced by methylation in somatic tissues are transcribed in the placenta [1,2,3,4,5]. The parallel hypomethylation of repetitive elements in the placenta and in cancer is just one of the many welldocumented similarities between placental and cancer cells. These two cell types share common molecular mechanisms that are thought to regulate their similar proliferative, migratory and invasive phenotypes [15]. The co-existence of genetically dissimilar fetal and maternal cells in the placenta echoes the interface of genetically normal and genetically abnormal cancer cells that occurs in neoplasms
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