Abstract
The Transcribed-Ultra Conserved Regions (T-UCRs) are a class of novel non-coding RNAs that arise from the dark matter of the genome. T-UCRs are highly conserved between mouse, rat, and human genomes, which might indicate a definitive role for these elements in health and disease. The growing body of evidence suggests that T-UCRs contribute to oncogenic pathways. Neuroblastoma is a type of childhood cancer that is challenging to treat. The role of non-coding RNAs in the pathogenesis of neuroblastoma, in particular for cancer development, progression, and therapy resistance, has been documented. Exosmic non-coding RNAs are also involved in shaping the biology of the tumor microenvironment in neuroblastoma. In recent years, the involvement of T-UCRs in a wide variety of pathways in neuroblastoma has been discovered. Here, we present an overview of the involvement of T-UCRs in various cellular pathways, such as DNA damage response, proliferation, chemotherapy response, MYCN (v-myc myelocytomatosis viral related oncogene, neuroblastoma derived (avian)) amplification, gene copy number, and immune response, as well as correlate it to patient survival in neuroblastoma.
Highlights
Neuroblastoma is a type of peripheral sympathetic nervous system cancer, affecting mostly infants and young children (95% of which are under the age of 5, and occurring 13% more frequently in males), which alters the growth and proliferation of neural crest cells [1]
These results indicated that Transcribed-Ultra Conserved Regions (T-ultra-conserved regions (UCRs)) are involved in various aspects of neuroblastoma progression
The differentiating agent all-trans-retinoic acid (ATRA) has been used to treat children with neuroblastoma; no information is available describing how T-UCRs play a role in neuroblastoma chemotherapy responses
Summary
Neuroblastoma is a type of peripheral sympathetic nervous system cancer, affecting mostly infants and young children (95% of which are under the age of 5, and occurring 13% more frequently in males), which alters the growth and proliferation of neural crest cells (precursor nervous system cells) [1]. LRogegyuolfamtioanligonfaTn-cUy.CRResguinlavtiaorniooufsTc-UanCcResrsinhavsarbioeuens cfaonucnedrsihnafsobuerepnoftoeunntdialinways, includfaotinutgrhepaolpttereornemtidaolitnewrtaeryreasg,ciitoninocnluosfdwitnhigethaplmrteoritReediNni-Ancotsed,riahncygtpiogenersnmewe[itt1hh7y]m,latitrRiiomNnAetosh,fyhClayptpiGoenrmisolefathnhydislsatotainotenthHoef3pC(rpHoG3mKios4ltmaenred3rse) gion of thelopcraotteedinn-ecaordtihneg tgraennsecr[1ip7t]i,otnrismiteetohfyltahteiopnrootfeihni-sctoodniengHg3e(nHe,3aKn4dmhey3p)olxoicaat[e1d3].nTeahrestehedatrtaanwscerrieption site of the protein-coding gene, and hypoxia [13] These data were obtained from 59 cancer cell lines and 283 primary tumors treated with or without 5-aza-2 -deoxycytidine, a demethylation agent [17]. The authors discovered that uc.338 negatively regulates TIMP-1 levels through direct interaction with the 3′UTR of TIMP-1 mRNA, suggesting that uc.338 acts as an oncogene [18] (Figure 2A). The authors used 293T and colorectal cancer cell lines (SW480 and HCT116) in the studies This was the first study to Nond-ceomdinognRsNtrAat2e01th9,e5f, u39nction of T-UCRs in negative regulation of mRNA by direct interaction at 3′U3ToRf 14 [18]. The authors revealed a novel model for the regulation of miRNA through inhibiting microprocessor-mediated recognition and cleavage of primary-miRNA [22] (Figure 2C,D)
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