Abstract
Pediatric solid tumors are a diverse group of extracranial solid tumors representing approximately 40% of childhood cancers. Pediatric solid tumors are believed to arise as a result of disruptions in the developmental process of precursor cells which lead them to accumulate cancerous phenotypes. In contrast to many adult tumors, pediatric tumors typically feature a low number of genetic mutations in protein-coding genes which could explain the emergence of these phenotypes. It is likely that oncogenesis occurs after a failure at many different levels of regulation. Non-coding RNAs (ncRNAs) comprise a group of functional RNA molecules that lack protein coding potential but are essential in the regulation and maintenance of many epigenetic and post-translational mechanisms. Indeed, research has accumulated a large body of evidence implicating many ncRNAs in the regulation of well-established oncogenic networks. In this review we cover a range of extracranial solid tumors which represent some of the rarer and enigmatic childhood cancers known. We focus on two major classes of ncRNAs, microRNAs and long non-coding RNAs, which are likely to play a key role in the development of these cancers and emphasize their functional contributions and molecular interactions during tumor formation.
Highlights
Reviewed by: Alessio Naccarati, Italian Institute for Genomic Medicine (IIGM), Italy Zexuan Zhu, Shenzhen University, China
We focus on two major classes of Non-coding RNAs (ncRNAs), microRNAs and long noncoding RNAs, which are likely to play a key role in the development of these cancers and emphasize their functional contributions and molecular interactions during tumor formation
It is clear that both miRNAs and long non-coding RNAs (lncRNAs) form integral parts of the biological networks known to be impaired in pediatric solid tumors. miRNAs such as let-7 and mir-34 are key regulators of many pediatric oncogenes including MYC, MYCN, RAS, and MET (Johnson et al, 2005; Wei et al, 2008; Buechner et al, 2011; Yan et al, 2012)
Summary
Solid tumors can originate from cells of any of the three germ layers, the ectoderm, mesoderm, or endoderm, and likely arise due to disruptions in the developmental processes of these precursor cells, leading them to develop cancerous phenotypes (Chen et al, 2015). Adult cancers often display a high occurrence of genetic mutations, whereas pediatric solid tumors tend to feature a relatively low number of genetic mutations This has led to investigations into alternative forms of gene regulation that may contribute to the emergence and development of cancerous cells in pediatric cancers.
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