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Homo sapiens (human) SWI/SNF complex antagonist associated with prostate cancer 1 (SCHLAP1) URS0000150780_9606

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SCHLAP1: SCHLAP1 is a long non-coding RNA (lncRNA) that has been found to play a role in prostate cancer. It recruits EZH2 and DNMT3A to repress the expression of multiple miRNAs, including miR-340-5p, miR-143-3p, and miR-145-5p, which in turn regulate DNMT3A expression (Huang and Tang, 2021) [PMC9755597]. SCHLAP1 is abundantly expressed in approximately 25% of prostate cancers and can help distinguish aggressive tumors from less aggressive forms of the disease [PMC5043609]. Targeting SCHLAP1 may be a potential strategy to disrupt cancer progression; however, its role in triple-negative breast cancer (TNBC) is not well understood [PMC8060801]. There is an 18-bp matched sequence between miR-198 and SCHLAP1, suggesting target-specific selectivity (Fig [PMC7844842]). Additionally, SCHLAP1 has been shown to interact with the SWI/SNF complex (PMC6056913). It has also been found to be highly expressed in metastatic prostate cancer cells and linked to disease progression [PMC5138831] [PMC9490455]. SCHLAP1 antagonizes the SWI/SNF complex to modulate gene expression in prostate cancer (PMC9741976). The mRNA levels of SCHLAP1 were examined in prostate cancer tissues from 40 patients, revealing its biological significance in the disease [PMC7844842]. LncRNAs like SCHLAP1 have been identified as critical players in prostate cancer development and progression [PMC5732923]. Furthermore, lncRNAs including SCHLAP1 have shown potential as diagnostic markers for prostate cancer [PMC6056913].

Genome locations

Gene Ontology annotations

Sequence

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GCUUUUAUGAGCUGUAACACUCACCGCGAAGGUCCGCAGCUUCACUCCUGAAGCCAGCGAGACCACGAGCCUACUGGGAGGAACGAACAACUCCCGACGCGCCGCCUUAAGAGCUGUAACACUCACCGCGAAGGUCUGCAGCUUCACUCCUGAGCCAGCGAGACCACGAACCCACCAGAAGGAAAAAACUCCGAACACAUCUGAACAUCAGAAGCAACAAACUCCGGACACGCCGCCUUUAAGAACUGUAACACUCACUGCGAGGGUCCGCGGCUUCAUUCUUGAAGUGAGUGAGACCAAGAACCCACCAGUUCUGGACACAAUUUCAAGUCCUCAGGUGCCAUCAAUAUUCUGAAAAUGGCAGUGAUUUUUAUUCAACCUGUAUAAGGCACUUUCACCAUGUACCUGGAAGCAACAUCUACAUCUUUUUCAGUUUCUUCUACGCCAGGUGUGUGCUUAGCUCCAUGACAAAAGGUGACAGCUUAUUCUGCAGCACACACACAUCAUCAAAGUGGGAGGUGGUGAGACUGGCACACUGACAGUCUGUCCUAGCAGAUUUCAGCUCACACUGCAAUCUAGAUGCUGGGGACACAAGGUCCACCUUCCAGGAAUAUGGCCAUGACACCAGAAAUCACAAACAUGAUGAGAAUGGAAUGACUGGGGAAGAAGUGCCAGAUGCUUCACUUGUAAAUGAAGACCCAGCCUCUGGGGAUGCAGAUACCACCUCCCUGAAGAAGCUGAAUAUCUGCAGAUAAGUGGAGUUCACCAAUGAUGAGGAGCGGGAUGGAGAAAGGAGGUAGGGAGAGUCAUCCAAGGAACAUGAGCAACAUGUUAAAAGCCAAGUGGUUUAAUUUCUGGAGAUGGUGAACCCAAGAGGCUCUGCUGGGAGACAACAAAAAUAAUGAAGAAUUGAACCAGAGUCCGGUGAAUAUCAGCACUGGGACCAGUUAGCAGAGGAAAAGGAAAGAAUAAAAGCGAAAAGAAUGAAGAGUCAUAUGAUUACCAACUUUUCCUUUUUCAUAUAAAUUGAGUGUAUAUGGGUCUGGAACAACCUGAAUUUCCAUCAAGUCCUGGCUAACCUCAUUAUGUCCUAUGAAUAUUUUUGACUAAUCCCACUUUACAUUAAUCUGUAUUGUGAAUGUGGAUAUUGAAUUAUAUUUCUUUGUAAUCCCAUUAUCCAAAAUCCAGUUCAGAGACUAUUAGUUACCAAUGUUCACUGUGAAGGAAAAAAAAAAAAAAAAAGCUCAGAGGAUAAACAUGUGAUAUGGUUUGGCUGUGUCCCCACCCAAAUAUCAUCUUGAAUUGUAGCUCCCAUAAUUCCCACGUGUUGUGGGAGGGACCCGGUGGGAGAUAAUUGUAUCAUGGGGGUGGUUCCCCCAUACUAUUCUCAUAGUAGUGAAUAAGUCUCACAAAAUCUGAUGGUUUUAUGAGGGAAAACCCCUUUCACCUGGUUCUCAUUCUCUUCUCUGGUCUGUCGUCAUGUAAGACAUGCCUUUCACCUUCUCCACCAUGACUGUGAGGCCUCCCCAGCCACGUGGAACUGUGAGCCCAUUAAACCUCUUUCACUUAUAAAU

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Publications