Abstract
BackgroundVestibular schwannomas are benign tumors that arise from Schwann cells in the VIII cranial pair and usually present NF2 gene mutations and/or loss of heterozygosity on chromosome 22q. Deregulation has also been found in several genes, such as ERBB2 and NRG1. MicroRNAs are non-coding RNAs approximately 21 to 23 nucleotides in length that regulate mRNAs, usually by degradation at the post-transcriptional level.MethodsWe used microarray technology to test the deregulation of miRNAs and other non-coding RNAs present in GeneChip miRNA 1.0 (Affymetrix) over 16 vestibular schwannomas and 3 control-nerves, validating 10 of them by qRT-PCR.FindingsOur results showed the deregulation of 174 miRNAs, including miR-10b, miR-206, miR-183 and miR-204, and the upregulation of miR-431, miR-221, miR-21 and miR-720, among others. The results also showed an aberrant expression of other non-coding RNAs. We also found a general upregulation of the miRNA cluster located at chromosome 14q32.ConclusionOur results suggest that several miRNAs are involved in tumor formation and/or maintenance and that global upregulation of the 14q32 chromosomal site contains miRNAs that may represent a therapeutic target for this neoplasm.
Highlights
Schwannomas are benign tumors that arise from Schwann cells in the peripheral nerves
The molecular hallmark of the disease is the biallelic inactivation of the tumor suppressor neurofibromatosis type 2 syndrome (NF2) gene by several mechanisms [2], such as mutation or loss of heterozygosity (LOH) of chromosome 22 where this gene is hosted (i.e., 22q12.2)
Contrary to non-head and neck schwannomas, sporadic vestibular schwannomas have shown no mutations on BRAF, EGFR, PIK3CA or KRAS [8]
Summary
Schwannomas are benign tumors that arise from Schwann cells in the peripheral nerves. These tumors often originate from the vestibular nerve, and they are histologically benign, vestibular schwannomas may cause hearing loss, tinnitus, facial palsy, and when large enough, brain stem compression and even death. The molecular hallmark of the disease is the biallelic inactivation of the tumor suppressor NF2 gene by several mechanisms [2], such as mutation or loss of heterozygosity (LOH) of chromosome 22 where this gene is hosted (i.e., 22q12.2). Vestibular schwannomas are benign tumors that arise from Schwann cells in the VIII cranial pair and usually present NF2 gene mutations and/or loss of heterozygosity on chromosome 22q. MicroRNAs are non-coding RNAs approximately 21 to 23 nucleotides in length that regulate mRNAs, usually by degradation at the post-transcriptional level
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