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Homo sapiens (human) DCST1 antisense RNA 1 (DCST1-AS1) URS000075A153_9606

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DCST1-AS1: DCST1-AS1 is a long non-coding RNA (lncRNA) that has been implicated in various cancer types, including oral squamous cell carcinoma (OSCC) [PMC8369177]. It has been shown to promote OSCC development by enhancing the NF-κB signaling pathway [PMC8369177]. In addition, DCST1-AS1 is activated by the MYC oncogene and is degraded by binding to miR-873-5p [PMC6930439]. It has also been characterized as an oncogenic lncRNA in liver cancer and colorectal cancer (CRC) [PMC6930439] [PMC8805871]. Bioinformatics analysis suggests that DCST1-AS1 may interact with miR-92a-3p [PMC7035894]. Furthermore, mutations in the miRNA-binding sites of DCST1-AS1 have been generated to study its functional effects [PMC8420713]. The study also revealed that the miR-582-5p/HMGB1 axis is a downstream target of DCST1-AS1, mediating its oncogenic effects in CRC [PMC8805871]. In summary, DCST1-AS1 is an oncogenic lncRNA that plays a role in OSCC development through NF-kB signaling pathway activation. It is regulated by MYC and miR8735p. It has also been implicated in liver cancer and CRC. Bioinformatics analysis suggests its interaction with miR92a3p. Furthermore, mutations have been generated to study its functional effects. The downstream target of DCSTl ASl includes the miR5825p/HMGBl axis which mediates its oncogenic effects in CRC.

Genome locations

Gene Ontology annotations

Sequence

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GCCCGCGCUGCUCAGCGCUACCGCUUCCCCGCAACUGUGCGGAGUGGGAGCCGGUGCCCGGUCCGACCGGCUUGGGCGGCGCGCCUUCACCCGGCGCCAGGUCCGGACCCCUCCCUAGUAGCUUCGCGGCCUCCCUGCCUCCUGUGCGCGGCCUGGCUCGGAGAGGUCGGGCGGGCAGGCUUUCCCGACUGCAGGCGAGGCAGUGCGCGGCUCACCCCAGUCCCCGACCCACGUGAAGCGUACAGGGCAUUUUAUUAACCGGGAAGGACGGUGCGGAAGAGCGAGCAGGACGCCUCUUCACCCCGCGUAGGCAGUGUCGUCGUUGCUGUCACUAAAGGCGGAGGAAGAGAGCUCUUCGCGGGGCGUGCAGACCGGGCACCGCUGCCGCAUGUCGUCCCAGCACGACCAGCAGUACACGGCCUCGCAGUCCAGCGUCCGGCACACGUAGGACUCGGGCGUCUCGGGUGCCUGGCACACCACGCAGCGCCGGCACAGCCAGCGGCGCAGGAGCGGGCAGCCGCGGUGCAGGAUAUCCGCCAGCGGGUGGCGCUGUUGGGAGGUGAGAAAACUGAUGCUUGGAGAUGUGAUCACUGCCCAGGGUCACCCAAUGAUAACAUGCAUGCAUAUGGAACUUGCUGCAUGCCAGCACCAUGAGUCCGCUCCCCAUGCUGUCCUCACCACAUUGCUCAUUUCUGAGGCCUGGAUGGUGGGCUUGCAAGGGAAGAUGACGGUUUUCUCCUCAGCUUUGCGGAGUGGCAGCAGAGUCCGUUUGCCCUGGAAAACAAAUGUCCACACAGUUAGGAAGCCCAAGGGCCCUCUGCCCUUUCCUCUCUGCCUUCCUGGAGCAUGAACCCACACAGGGCACACAGCAGCAAGGCAUCCCCGGGCAGUGCCGUGCCCACUCACCAGCUUCUUCCUGCGGUCAUCGAUCUGGCAGAAGUUCUCCUCAUCUAUCCCCAAACAUGGGCUUCCUUGAGGCACAGUCAUUCAACCAACCAGCCAGCAUUCAUUGAGCACCAUCUAUGUCCUGGGCACUGCUAGGGGAUGGUGAUAACAGGGAGAAGACUCUGUCCCUGCCUUCCAAUUGUGUAGAGGAAGACAUCCCCCUACAUGAUGGGUGAGACAUAGCAGAAGUGAGUAGGGGAUGAGGUGGGGGCUCAGAGGAGGGCAUGGUCAGCCUGUCUGGGAGGGAGUUGCAUGUGUGCAUCUGAGGUAGGGACAGGCAUGCAUCUUACAGGAUGAAUAUCGAGCAGAGUUACAGAGAGGGGGAAACUCCUUGAGGUUUCAGGAAUCACCUAAUCCACUGUGACUCACAAAUUCCUGCCUCUUGGCUUUGCCUGCAGCAUAUCUCCUGGAAGUGUGCUGGGGCAAAACUCAUCCCAGACCACCAUCUCCAUCCUCCCCCAAUACACCCUGGCUCUCCCUGGCUACCCUUGAGCACGGUGCACGUGUGCAUGGGUGCAUGCCUGCAUAUAUAGCUAUCCCCCAUGUAUUUCCCAAAGCCCUACAUAAUGCUUCAGUUUGCUAAGGAAAAAAUGUUAAUUACUGCAAAUGUGUUUAAAACUGUAAAAGUACAUUAAACAAACUCUGUAAAGUGUGAAAAAAAAAAAAAAAAAA

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Publications