v24

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Homo sapiens (human) ID2 antisense RNA 1 (ID2-AS1) URS000075DDF2_9606

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ID2-AS1: ID2-AS1 is a long non-coding RNA (lncRNA) that acts as a chromatin modifier to regulate ID2 transcription by controlling the binding of H3K27ac to the ID2 promoter and RNA polymerase II (RNAPII) to the ID2 enhancer domain [PMC9716033]. Downregulation of ID2 using ID2-AS1 inhibits hepatocellular carcinoma (HCC) invasion and migration in vitro and in vivo by blocking HDAC8 occupancy at the ID2 enhancer region [PMC9563588]. RT-qPCR validation confirmed the expression of several mRNAs and lncRNAs, including ID2-AS1, in HCC [PMC9327205]. Functional experiments have shown that lncRNAs such as MYCNOS, NEAT1, and SNHG11 promote HCC cell proliferation, migration, and invasion, while MAGI2-AS3, ID2-AS1, and HHIP-AS1 have opposite effects [PMC8442226]. In HCC, ID2-AS1 suppresses tumor metastasis through the HDAC8/ID2 pathway [PMC9158467]. In addition to its role in HCC metastasis suppression, ID2-AS1 has been found to regulate chromatin modification and inhibit epithelial-mesenchymal transition (EMT) in bladder cancer (BLCA) [PMC10135817]. High expression of ID2-AS1 is associated with better overall survival in BLCA patients [PMC9239636]. Furthermore, high expression of ID2-AS1 is correlated with better immunotherapeutic response in BLCA patients [PMC9239636].

Genome locations

Gene Ontology annotations

Sequence

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GAGCCCAGCUGGGGUGGUAAAUAGAGUACAGUACAAAAGCGGAAGGGGCAGGCCUAGAAGCUGAAAGAAAAGCUCGAUAAUGGGGAAACAGUGUUUUUUCCUUCAAUUAAUGAUUAAUUUCUCAGCUGGUGGGGCCAGCAGUCUCUGACCGUCACGUGACAGCUAUGCGCCCCAUGACGCCUCUCCAGGGAGGCAGAGUGGGUGGCACUGAGGUGGAGCUCACCUUCCUGAAAUUCAGCCCCCUCAGUUUGGAGGAAGGAGGUAAACUGUUUCCUGUCCAGCCAGAAGUUUGCGGAGGGCCUUCCCCAGGCCAGGCAAUGCUGCCUGCGACUCUGUCCCUGACAGCGUUGGAUGCACCGUAUCUCUUCUGAUAUUAAGUCUGGAAGUGAUUUACUAUCCGAGUCCUCCCACAGUUCGAGCCUUUUGAUGUACUUUGUGUGCAUGUGUUUCUGUCACAUACGUGCCACAGUGGAACAGAUUUUGUUUUGACACUAUUUUGGUUCAUGAUGUUAUACUUUGACUAUUUUACAAUAAUAGCCAAUGUAAACAAACAUCUUUGGGAUUCUCAAAUUAUUACUUAUGAUUCUUGGACAUUGCAGCUCUUCGAUACUGACGCAUUCCUAGCUUUUUCCAAGGACACCGUAUGUUAACAUCCGUGCCAGCCUCAUUAUCCCCACAGCCAGGCUCUGGGUUGGGCGGUAAUGAGCAUUGUGCGGUUUCACUUUACACUUUGCAAAGUUGAUUAAGGCAGUGCCUUCUCCCAUGAUCAUUUUUGUACCCUGAUGUAGUAAAAUGGCUAAAUAUGGUGAAAGUUAAAAAAAAAAAA

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Publications