Abstract
MicroRNAs (miRNAs) are key molecules that regulate biological processes such as cell proliferation, differentiation, and apoptosis in cancer. Somatic copy number alterations (SCNAs) are common genetic mutations that play essential roles in cancer development. Here, we investigated the association between miRNAs and SCNAs in cancer. We collected 2538 tumor samples for seven cancer types from The Cancer Genome Atlas. We found that 32−84% of miRNAs are in SCNA regions, with the rate depending on the cancer type. In these regions, we identified 80 SCNA-miRNAs whose expression was mainly associated with SCNAs in at least one cancer type and showed that these SCNA-miRNAs are related to cancer by survival analysis and literature searching. We also identified 58 SCNA-miRNAs common in the seven cancer types (CC-SCNA-miRNAs) and showed that these CC-SCNA-miRNAs are more likely to be related with protein and gene expression than other miRNAs. Furthermore, we experimentally validated the oncogenic role of miR-589. In conclusion, our results suggest that SCNA-miRNAs significantly alter biological processes related to cancer development, confirming the importance of SCNAs in non-coding regions in cancer.
Highlights
MicroRNAs are small, single-stranded non-coding RNA molecules, 17–25 nucleotides long, that act as post-transcriptional regulators of gene expression by binding to complementary sequences in the3’ untranslated region of target messenger RNAs [1,2]
Several studies showed that mir-31 and CDKN2A are concurrently deleted in cancers [41,42]. These results suggest that co-deletion of hsa-mir-491 and CDKN2A plays an important role in bladder carcinoma (BLCA), lung adenocarcinoma (LUAD), and uterine corpus endometrial carcinoma (UCEC), and that co-deletion of mir-31 and CDKN2A is a crucial event in BLCA and lung squamous cell carcinoma (LUSC)
We aimed to examine whether miRNAs tend to localize to Somatic copy number alterations (SCNAs) regions in seven cancer types
Summary
MicroRNAs (miRNAs) are small, single-stranded non-coding RNA molecules, 17–25 nucleotides long, that act as post-transcriptional regulators of gene expression by binding to complementary sequences in the3’ untranslated region of target messenger RNAs (mRNAs) [1,2]. MicroRNAs (miRNAs) are small, single-stranded non-coding RNA molecules, 17–25 nucleotides long, that act as post-transcriptional regulators of gene expression by binding to complementary sequences in the. MiRNAs have been investigated as key molecules involved in regulating important cancer-associated processes, such as cell proliferation, differentiation, and apoptosis [3]. Specific miRNAs were identified as biomarkers affecting the expression levels of genes involved in cancer development [4]. Genome Atlas (TCGA) datasets containing data for 12 cancer types and showed that members of a microRNA superfamily, including miR-17, miR-19, and miR-130, co-target critical tumor suppressors. Because of their important roles in cancer, it is important to understand the regulation of miRNA biogenesis. The regulation of miRNAs has been evaluated at different levels, including in studies of genetic mutations, epigenetic modifications, and alterations in the microprocessor components, such as DROSHA, DGCR8, and DICER1 [5]
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