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Homo sapiens (human) KDM4A antisense RNA 1 (KDM4A-AS1) URS000075DBBD_9606

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KDM4A-AS1: KDM4A-AS1 is a hypoxia-induced long non-coding RNA (lncRNA) that is highly likely to bind and stimulate the de-ubiquitination of androgen receptor (AR) in triple-negative breast cancer (TNBC) cells [PMC9408190]. It is one of the identified pyroptosis-related lncRNAs, along with ZFPM2-AS1, LUCAT1, NRAV, AL031985.3, AL049840.5, MKLN1-AS, AC099850.3, and LINC01224 [PMC9195296]. KDM4A-AS1 functions as a competing endogenous RNA (ceRNA) by sponging miR-411-5p [PMC8668937]. The chromatin immunoprecipitation assay showed that hypoxia-inducible factor 1-alpha (HIF-1α) directly binds to the hypoxia response elements in the KDM4A-AS1 promoter [PMC8668937]. The expression of KDM4A-AS1 has been explored in hepatocellular carcinoma (HCC), where it acts as an oncogene and may serve as a prognostic marker and potential therapeutic target for HCC [PMC8668937]. References: [PMC9408190] - Liu YR et al., 2020. Hypoxia-induced lncRNA KDM4A‑AS1 promotes the progression of triple-negative breast cancer by binding to USP14 and stabilizing AR. Oncol Rep. [PMC9195296] - Liu Y et al., 2020. Identification of pyroptosis-related lncRNAs for predicting prognosis and immunotherapeutic response in hepatocellular carcinoma. Front Oncol. [PMC8668937] - Zhang Z et al., 2021. LncRNA KDM4A-AS1 promotes hepatocellular carcinoma progression by acting as a ceRNA for miR-411-5p to regulate YAP1 expression. Aging (Albany NY).

Genome locations

Gene Ontology annotations

Sequence

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GAGGUUCGCGCUGGUGGAGCACCCCAGCUUGCAGGUUCAGCGUGGGUGUCUCUCCCGGGCACAUCGAGCUGUCUAGAGGAACCCUCUUCCCCUGGCUUCACGGCCCAGAGGACGCACGGCUCUCUCCCCUCGAGAGCGUGUUUCGUCGCCCGCGCGGGGAACGCAAAGUGCUAGGGUAGUCACGGCCACUUCACGCCGAGGGACAUCUCAUCUCGCCCUCCAGGUCGUGAGCGCACCCAUUCCGCUCACUGAGGCCGAAAGCUUCGGACCUCCGUGGGCCCUGAGACUUCAGCGUUCCAUGUCUGCUGUGCUGUGGAACCCAGAGUGCUCUUGCCUGGAUGGCUGAGAAUCCCUUGGACCCUGGAAGCACCUACUCCAUGAUGGCCCGCAGGAGGACCAAACUGGAGACAGUCCUGGCUCUGAGGAAACAGGAAGGAAGGAGGGUGAAAGGAACGUCCACCUGCACACAAAGGAAAGAUGAAAAAGAGUCACCUACCAUGGGACCUGGCAAAGUACUUCAGAACUUUUAUUCCUUCCAGAAGCAGAUUCCACACUGCAACUAACUUUUAAGAACCUGCCAGGAGCAGUGGCUCACACCUGUAAUCCCAGCACUUUGGGAGGUUGAGGCAAAAGAAAUCGCUUGAGCCCAGGAGUUUGAGACUACCUGGGCAAGAUGGCAAGACCCCAUUUCUACAAAUAGCCAUGCAUGCCUGUAGUCCCAGCUACUCGGGAGGUGCUUGGUCAACAAAGCAAGACAUCAUCUCUUAAAACAAACAAACAAACAAAAAAAGUUGUUACUUCCAUUGAGUUUUGGUGGAUAUCAGAGAAUAAUAAACACAAUUACCUGAAAGACUAUUAAAAUACCUCCCUUGGCUGGGAGUGGUGGCUCACAGAUGUAAUCCCAGCACUUUGGGAGGCCGAGGUAGGCGGAUUGCUUGAGCCCAGUUUUGAGACCAGCCUGGGCAACAAGGCAAAACUCCAUCUCUACAAAAAAUUAAAAAAUUAGCUGGGCGCCAGUGACAAGGGCCUGUAGUCCCAGCUACUUGGGAGGCUGAGGCAGCAGAAUCACUUGAGCCUGGUAUGUGGAGGUUGCAGUGAGUUGAGAUCACUGCACUGCACUCCAACGUGGGUGACUGGAGUGAAACCCUAUUUUAAAAAAACAAAAACAAACUCCUUUUUCCAAUUACAUAUCUACGCAAGGCUGAAUUUUCUUCCUAUACUUGAACCUAAACAGUGUAUCACAAUAGAUUGAAUCAAGAAGUGACAUUAAGGCCAGCGCGGUGGCUCACGCCUGUAAUCCCACCACUUUGGGAGGCCGAGGCGGGCGGAUCACGAGAUCAGGAGAUCAAGACCAUCCUGGCUAACAUGGUGAAACCCCAUGUCUACUAAAAAUACAAAAAAUUAGCCGGGCAUGGUGGCGGGCGCCUGUAGUCCCAGCUACUCGGGAGGCUGAGGCAGGAGAAUGGCGUGAACCUGGGAGGUGAAGCCUGCAGUGAGCCAAGAUCAUGCCACCGUACUCCCGUACUCCAGCCUGGGCAACAGAGCAAGACUCCAUCUCAAAAAAAAAAAAAAAA

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Publications