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Homo sapiens (human) androgen receptor negatively regulated lncRNA (ARNILA) URS000076315D_9606

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ARNILA: ARNILA is a long non-coding RNA (lncRNA) that acts as a competing endogenous RNA by sequestering miR-204, leading to increased expression of its target gene, SOX4. This upregulation of SOX4 promotes epithelial-mesenchymal transition (EMT), invasion, and metastasis in triple-negative breast cancer (TNBC) [PMC8799054]. In AR+ carcinomas, ARNILA is suppressed by dihydrotestosterone (DHT) and the androgen receptor (AR), resulting in decreased miR-204 binding and inhibition of SOX4 expression [PMC6433747]. ARNILA is located in the cytoplasm of TNBC tissues and cells, where it has been shown to promote invasion, EMT, and metastasis in both in vivo and in vitro experiments [PMC6555305]. In breast cancer, lncRNAs have dual roles. Some lncRNAs act as tumor suppressors, such as MEG3 and ANCR. On the other hand, lncRNAs like ARNILA contribute to cancer progression [PMC8230351]. Additionally, certain lncRNAs like GAS5 can directly regulate EMT pathways and TNBC invasion by functioning as competing endogenous RNAs for EMT-regulating RNAs [PMC6521131]. Overall, ARNILA plays a significant role in breast cancer progression by competing with miR-204 for binding to SOX4 mRNA. Its suppression by DHT/AR signaling further enhances the expression of SOX4. Understanding the mechanisms involving ARNILA can provide insights into potential therapeutic targets for TNBC metastasis [PMC9468319].

Genome locations

Gene Ontology annotations

Sequence

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GAUCUUAGUUCAUCUCUUUAGGAUUGGGAGGGUCAGGAAGAAAAAGAUCUAGCUACGAUAAUAGACAUUCUUUACAGAUGCAAAUUUUCCCCCCACAAAAAACAGCUUUGUGCAGGGCCUUUUCAAAAUAUGGCAAAGAAACAUGUUUUGGGGUAAAAUAUUUUUAUUUUCUUCCUUGUCUCAUAACGUUAUGCCAGCCAGAGUCAGGCUGGAAAGUAAGUCACAAUAUAUAGGGUUAAAUGAAACCUAUCUGAUGAGAAUUUAUGAUUUGUAGGGCAUGACUCUCCAGACCCCUUAGAUAGGAAUUUGGGCAAGAUAAAAAAAAUCAGAGUUUAGUCCUCACCACAGUGUCAACUUGCUAAUGUGAUGGAAUGGCAGCAAGAUUUCAAAGAAGAUUUUGGGGGAGAGAGCAGGGAGUGGCUCAGGGAAAGAAGUGGAGUGUUGAGUCAGUUGGCUUAAUGGGAACCUGGUUUGCCCAUUUUGAAAACCACAACGGAGAAAUAAUCACCCAGAUCUACUAUUUUUUCACCUUAAAACAUCCUGGGGCCCGUCAUCUUGCACCCUGGCUCUGCAGGGCAGGAUUGGAAGGUCUCUGGGGGGCCCCGCUCCUCUGAAGGAUCACCUGCCCCACCUGUCACAUUCCUCCCUGGCCAGGCCUCACACUAAAGAGACUCGCCUGGCUCCACCAACACCCACUCCAGACUCUGUAGGGGGGUAUCAGCAGAAAUUGAAUCUUUAGCCCCACAGAGAGGCUGUGACAUUCCCACUGCCACUUAAGGGUUAGGGCUAGUCAGAGAAUCAUAGAACGUUAAAGUGUGAAGGAACCAUCAGGACAGCUCAAGAAGCCGAAACCAAGCAAAUCAGAUGGCCCAGGGCCACACAGGGAAGGAGUGGAGGGGUCCCUGCGGGAGUGCUGCCCCUUCCAGGCCUCCUCUGUCACCAGAGGAGCUGGUCCUGCUGCUUAGAGUCAUAUUAAACCUUUGGAUGGGGUAUGUAAGGACACUUUCCCCUGGAAAAAUGCUACGUCACUCACUUUAUAUCCUGGCCUUAGGCCAACUGAGCCUUCACCCCACCCUCCCUGCCUAAGUCACCUCACCAAGCAUCCUCUGGUACUGACGACGAUGCUUUUGGCCUGGUUACCAAGCUUUCCUGACCACCUGAUGGUAGGGCCCCUCCACAUGGGCUAUUCAUCCUCCCAGAAGCAGGUCCUCCAGUGACUGAUCUGCACUAAUGUGGGCAAACAGAGGGCAUCCUCCUCCUCUCUCUGCUUCUUUUCUUUGCAAAAUUAGUGGGACAAAUAGGUACAAGUUGCAUGAAAAUGAGAUACAGUUCUUCAUUUGCCAUCCACACCAGGAGCACCAGGUCCCGGAGCCCAGCUGUGCAUUAGAUGUUGUCUCUGCAGCACAAGGUAGGAGGCUGCAGGAUGUACCUGAGAAACGCAAUCGCACAAAGCAAUUGUUCAGCACCAAAUAUGGGGGACAGAAGAGUGCUAAGGGGAGAAGACUCCAACCAUAAAUAAAUAAAAUGGCAGCAAAUUAGGAAAUAACAGAAA

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Publications