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Homo sapiens (human) long intergenic non-protein coding RNA 1014 (LINC01014) URS000007FFF1_9606

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LINC01014: LINC01014 is a long non-coding RNA (lncRNA) that has been implicated in various aspects of esophageal squamous cell carcinoma (ESCC) pathogenesis and drug resistance [PMC9031703]. It has been shown that LINC01014 is associated with the PI3K/Akt/mTOR pathway and is specifically involved in gefitinib drug resistance in ESCC [PMC9031703]. LINC01014 has been found to resist the efficacy of gefitinib, a targeted therapy, suggesting that it requires attention in terms of prognosis and therapy in clinical settings [PMC9031703]. Mounting evidence suggests that various lncRNAs, including LINC01014, are involved in ESCC chemotherapy resistance [PMC9031703]. Overexpression of LINC01014 has been shown to confer gefitinib resistance by inhibiting apoptosis through the PI3K/Akt/mTOR signaling pathway [PMC9031703]. Silencing the expression of LINC01014, on the other hand, promotes apoptosis induced by gefitinib treatment [PMC6991649]. The expression of LINC01014 can be determined using RT-qPCR with GAPDH as an internal control [PMC6991649]. It has also been found that overexpression of LINC01014 increases the expression of PIK3CA and Bcl-2 while decreasing the expression of Bax, suggesting its role in inhibiting apoptosis [PMC6991649]. In summary, LINC01014 is an lncRNA associated with drug resistance and modulation of the PI3K/Akt/mTOR pathway in ESCC. It plays a role in inhibiting apoptosis and altering sensitivity to gefitinib treatment.

Genome locations

Gene Ontology annotations

Sequence

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GUCUCCAGGGCACGUCUUUUCUCCUGGGUUUCUAUGUUUGUUUUACUCACUGCCUCUCGUUCCUCUGCUUACGACAUUUUCAUGAAUAAGCCAGAAGAUAGUCAGCACAGAAGCCUCCCUACAACCUGGAAAAAGAAAUGAGCUUUCACUUUGAAUAUCACACAGACAUACUGAGGUGGGAAACUACAUGUGCGUGCUUGACACAACUUGAAAACAAUACAAAACAACAAAUCACAAUUGCAAAAUCAUACAACACAAAUGGAAUCACAGUCCAUAAGGGAGGCCAUGAAAGAGAGAGUGCAUGUGGUGGACAUAUUAAGCUGAUAUGCAGACCUGGGAUGGUGUCAGACAAGUGCUGAAGGCACUGUUUGUUUCCUGCCCCAAUGCUGAGCUCAGACCACAACCGAAUCCAGAGCCUGCCAUUUAUCACUUGACCACGUACAUCUGAACCUGCAAGACCCUCGCACAGCCUUCACUGAGGUGUGAAAACUGACAGUUUCCUUCUCCUGCCACUGGUUCUGCAGUAAUUAAAGCUUUUUUGCUAUCGC

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Publications