Abstract
MicroRNAs are key regulators of gene expression and have been shown to have altered expression in a variety of cancer types, including epithelial ovarian cancer. MiRNA function is most often achieved through binding to the 3′-untranslated region of the target protein coding gene. Mutation screening using massively-parallel sequencing of 712 miRNA genes in 86 ovarian cancer cases identified only 5 mutated miRNA genes, each in a different case. One mutation was located in the mature miRNA, and three mutations were predicted to alter the secondary structure of the miRNA transcript. Screening of the 3′-untranslated region of 18 candidate cancer genes identified one mutation in each of AKT2, EGFR, ERRB2 and CTNNB1. The functional effect of these mutations is unclear, as expression data available for AKT2 and EGFR showed no increase in gene transcript. Mutations in miRNA genes and 3′-untranslated regions are thus uncommon in ovarian cancer.
Highlights
MicroRNAs, a class of small non-coding RNA molecules, have important regulatory roles in diverse cellular pathways including proliferation, differentiation, senescence and metabolism [1]. This regulation is achieved through semicomplementary base paring with the 39-untranslated region (39UTR) of the target messenger RNA [1,2,3], as well as the 59-untranslated region or coding regions of mRNAs, which are subsequently degraded or post-transcriptionally silenced [4,5,6]
Somatic mutations targeting microRNA genes are infrequent events in ovarian tumors To investigate whether mutations in miRNA genes contribute to altered miRNA activity in ovarian cancer, 86 primary epithelial ovarian tumors were assessed for somatic mutations in genomic regions corresponding to precursor or mature miRNA sequences
Somatic mutations were detected in 6% (5/86) of tumors and in less than 1% (5/712) of miRNA genes analysed, with no miRNA genes recurrently targeted by mutation
Summary
MicroRNAs (miRNAs), a class of small non-coding RNA molecules, have important regulatory roles in diverse cellular pathways including proliferation, differentiation, senescence and metabolism [1]. While germline alterations at miRNA binding sites in 39-UTRs may contribute to cancer susceptibility [11,15,16,17], reports of somatic mutations occurring in a similar context is limited to a single case report [13] and has yet be to investigated in large tumor cohorts.
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