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Homo sapiens (human) SPANXA2 overlapping transcript 1 (SPANXA2-OT1) URS000075B855_9606

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SPANXA2-OT1: SPANXA2-OT1 is a non-coding protein whose function is not yet known [PMC7779438]. Increased expression of SPANXA2-OT1 in NPC samples suggests that NPC cells experience inhibition of the apoptosis process, leading to increased cancer cell proliferation [PMC7779438]. SPANXA2-OT1 is involved in the apoptosis signaling pathway, along with GCK and PRKCG [PMC7779438]. SPANXA2-OT1 has been upregulated in a study [PMC7779438]. According to PANTHER, SPANXA2-OT1 plays a role in the signaling pathway of the BCL-2 protein group, which functions as an anti-apoptotic protein [PMC7779438]. Several non-coding RNAs, including SPANXA2-OT1, are directly linked to various cancers [PMC9327231]. The expression of SPANXA2-OT1 was significantly upregulated after 48 hours of COM stimulation compared to the control group [PMC8502877]. The interference efficiency of small interfering RNA targeting lncRNA SPANXA2-OT1 was determined by RT-PCR for subsequent experiments [PMC8502877]. A firefly-sea kidney dual-luciferase reporter gene assay confirmed that lncRNA SPANXA2-OT1 could bind to miR-204 [PMC8502877]. Functional experiments showed that lncRNA SPANXA2-OT1 could promote cell apoptosis and inhibit cell proliferation [PMC8502877]. The miR204 inhibitor could alleviate the interference effect on lncRNA SPANXA2-OT1 and promote the occurrence and development of EMT in renal tubular epithelial cells by increasing Smad5 expression [PMC8502877].

Genome locations

Gene Ontology annotations

Sequence

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CUGUUAGAAGCCCGGGGUUAUGGAAGAGAAGCGUGGAAACCAGCGACCAGCGUUCAGGUAGAUUAGGACCAACCCCGGCACUUAGCUGCACAGGAACAAUGGCGAGCCCCUUUGGGCGCCUCACUGAUCAGAAGGGCAGAGGACACCCUGCUGGAUCUGGAGGAGUGGAAGUCAAUGGCGGGUCUGCGAGGGCGGCGUUCAGCGGUGGUGGACGGAGGGUGUUGAGCGGUGGUGGACGGUGGUGGACGACGGCCUUCGGCGGUGGUGGACGGACGGCCUUCGGCGUUGGUGGACGGACGGCCUUCGGCGGUGGUGGACGGACGGCCUUCGGCGGUGGUGGACGGACGGCCUUCGGCGUUGGUGGACGGACGGCUUUCGGCGGUGGUGAACGAGUCUCACUCUUGUCACCAGGCUGGAGUGCAUUGGCGCGAUCUUGGCUCACUGCAUCCUCUGCCUCCCGGGUUCAAGCGAUUCUCCUGCCUCAGCCUCCCGAGUAGCUGGAACUACAGGUGCUGGACAAAGAUCAGACCAGAUGUGAGGAAUGCUGAAAAUGAAAGUCUCUUCUGAUAUGUUCACCAAAGAAAGCGAUCCCUUAGCCCAGAUCUUGGCAAGAACCAGUGUCAAAGGGAUGUUCAUCCAGUAAUCCUGAAUUGUUGGACACCCAAGAAGAGAAUCAAGAUGAAAAUCUGUGCAGUUCUGUGAGAUUUCUGUAGUACUUUGUUCUGCUUACACUUCAAAAGCAAGCUAGACUUUCAACUUAGUAUAGCAUUGUCAUUUCCACUGAUGUAUUUCCUGAGUAUAGAUACCAACUCUCCUGAUUUCCUCAGGACUAAAGGAGUUUCUGGGACAAGAAAAUUAUAGUUUUAAAAACAGGACAGCCCCAGCAAACUGGGACAAGUUGGUCACACUAUGCAUGAGGAUGUGUAUAUAUGCAUAUUUUUAUGUAUGCUAAUUCAUAUUAUAAUUUACAUACCAUAUUUAUACUAGGAAUCAGGUGUGUUAAAUCCCAUGAUACACAUAUGUUUAUACUCCAAAAUCUAUGUAAUUACCAUCUAUUUCUAAAAAACAUUCUAGAAACAAAAGUAAUUAUGAAAGGCUAUUUUACUAUAUUUUGGACCAUAUAUCAUCAUACCAUAUUUAGGACCUCAUUUGUUAAGGCUAACUACCUGAAUAUCUUGAGCAGCCACAAGUUUAGCCCAUUUCAUGGGACUCAUUAUAGCAAGUGUUCAUUUCUCCCACCCUCUGUUCAUGUCCCCAGUUAUAUGAACAGGAAUUUUUUGUUAGAAUAGAACAAAUUCUUUAUUUUUGCUAUGUUACAGAUAAUGGAAAAGCUUGCAUACAUGGCCACUUUGGAGGAUAGACACUUUUCCUCAUUUAACAAAAUAGUGUGAAUACAUAAGACCAUGCCAUCAUUUUUAUUAAUCAAAGCUGUUACCUUUUCUGAAAGAAUUGUUCUAUUUCCUUGAGCUCAUUGUGAUGAAUCUUGAGUCUCCCCUCAAGAAUUAAGCUGUGUUCUGGAAGAUGAAAAGCAGCCCUCCCCAAAGUUAUACCAAGACAUAUUGGAAUAUGCUUUUCUAUUAUAUCUAGAUAUCUGGAUGGAAAAAUUAGACUGGGGAUUUAUUUUAAAAAGAGAGACAUUUCAUACUUGGUAUUUGAAAAUACGCUAGCACAGCUCUUGGAAAUAAACAGUAAUCUAAC

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Publications