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Homo sapiens (human) RBPMS antisense RNA 1 (RBPMS-AS1) URS000075B634_9606

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RBPMS-AS1: The expression levels of various lncRNAs, including RBPMS-AS1, were analyzed in different risk groups of GBM patients, and the heat map analysis revealed that RBPMS-AS1 had higher expression levels in the low-risk group [PMC8448051]. RBPMS-AS1 has been implicated in glioblastoma multiforme (GBM) cell proliferation and radiotherapy resistance through the miR-301a-3p/CAMTA1 axis [PMC8605343]. This suggests that RBPMS-AS1 may play a role in reducing GBM cell proliferation and enhancing sensitivity to radiotherapy in low-risk patients [PMC8448051]. The specific mechanism by which RBPMS-AS1 exerts its effects is through the miR-301a-3p/CAMTA1 axis, involving the interaction between RBPMS-AS1 and miR-301a-3p, which leads to the regulation of CAMTA1 expression [PMC8605343]. Targeting this axis may hold promise for developing therapeutic strategies for GBM patients with high-risk profiles [PMC8605343]. Overall, these findings highlight the potential importance of RBPMS-AS1 as a therapeutic target for GBM treatment [PMC8448051].

Genome locations

Gene Ontology annotations

Sequence

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AUUAUACUUACAAAAGUCUCCGAAAAGUCCUUGGAGUUACGCAAUUUGGGGCCCGCAGACGCGCGUGGACACAAAAACACACGCUCCCGAGAUCCACCCUCCCCGGGCCACACUGUGGGGCUGCGUCCGGGGCACGGGCCAUGCCUGAACCUUCUUCCACCGCCGCGCCCCGGGCCCGCGCCCCGCCGGCCGCCCGCACUGGGUCCCGCGUCGCCCCCGCCACCACACCGAGCCGCCCAGUACCUCCUCCUCCUGAAGGCAGAGCUGGGGGUCCGUACGGAGGAACUUCAGAGGCUGGAAGCACGCUUGAAAAAGAAAGGGGGCCUGGGCUUUGCACCAGCUUCAGGAUUGCGUACUUGUUUCCUCAUCCGUGAAAUGGGAGCAGCUGAAUGUGUCUCCUCGAGUUUUCGAGGGGAACAAACAUGUAUCCUGGAUGAAAAUAAACCAACUCUUGAAACUGCAACCCAAGACAUUCAGAAGAGAUAAGGCUACAGUGAAUGUGGAAACUUUGCACGUGUUUGGAUGUAUUGAUUGCCUUAACUGGCAGCUCUUUGCACUGCCAGCUUCCCUCAAUUACAUGAGGAACCACGAGGGGGCAAUGUCUUCCCGAGCAAUAAUAGCUGAGUGGUGGUCUUAGGACCCCGUGGUGGCCCAUGAUGCUAGCACUGUGUCUUUGGCCAUUCUUGCCUGUCAUGGAGCAUACUCCACAGAAGGGCAUGGUCUUCUUGGAUCCCGGCAUGGGCCCAACAAAAAUGACAAUGUAGUCAAUAGUUCCACUCAGACCUCACUUAGGAGCAGGUGAACUAUGUUGUGUGAUAUCAGGAUGCCCGGAGAACCUCUCCUAUCCCCACCCAGGGAAGCAUGGCUUAAUUCCAAAUAAAGAAUCUGAUUUCUUUGUCUUUAAGCCAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA

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Publications