Knockdown of lncRNA HIF1A-AS2 increases drug sensitivity of SCLC cells in association with autophagy

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dc.contributor.authorGuclu, Ebru
dc.contributor.authorGunes, Canan Eroglu
dc.contributor.authorKurar, Ercan
dc.contributor.authorVural, Hasibe
dc.date.accessioned2024-02-23T13:59:47Z
dc.date.available2024-02-23T13:59:47Z
dc.date.issued2021
dc.departmentNEÜen_US
dc.description.abstractThe aim of this study was to determine the effect of lncRNA HIF1A-AS2 on autophagy-associated drug resistance in small cell lung cancer (SCLC) cells. The expression of HIF1A-AS2 was silenced by siRNA in doxorubicin-sensitive H69 and doxorubicin-resistant H69AR cells. Then, cytotoxicity, apoptosis and autophagy analyses were carried out in the normoxic and CoCl2-induced hypoxic environment. The effect of HIF1A-AS2 on the expression levels of genes, which are associated with drug resistance and autophagy, was determinated by qRT-PCR analysis. The levels of MRP1, HIF-1 alpha and Beclin-1 were analyzed by western blot method. Knockdown of HIF1A-AS2 increased doxorubicin sensitivity of SCLC cells and decreased autophagy. Knockdown of HIF1A-AS2 has also affected the expression of several genes that will increase drug sensitivity and inhibit autophagy in both cell lines. The levels of HIF-1 alpha and Beclin-1 were decreased in both cell lines by knockdown of HIF1A-AS2. MRP1 expression was decrease in H69AR cells. In addition, CoCl2-induced hypoxic environment decreased in doxorubicin sensitivity of H69 cells, and knockdown of HIF1A-AS2 reversed this effect of hypoxia. Knockdown of HIF1A-AS2 increased drug sensitivity of SCLC cells in relation to autophagy. Therefore, hypoxia-HIF1A-AS2-autophagy interaction is thought to be determinative in drug sensitivity of these cells.en_US
dc.description.sponsorshipNecmettin Erbakan University, Scientific Research Projects [181418001]en_US
dc.description.sponsorshipThis study was produced from the PhD thesis of Ebru Guclu and supported by Necmettin Erbakan University, Scientific Research Projects (#181418001).en_US
dc.identifier.doi10.1007/s12032-021-01562-2
dc.identifier.issn1357-0560
dc.identifier.issn1559-131X
dc.identifier.issue9en_US
dc.identifier.pmid34378101en_US
dc.identifier.scopus2-s2.0-85112251366en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1007/s12032-021-01562-2
dc.identifier.urihttps://hdl.handle.net/20.500.12452/11324
dc.identifier.volume38en_US
dc.identifier.wosWOS:000683719300001en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherHumana Press Incen_US
dc.relation.ispartofMedical Oncologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAutophagyen_US
dc.subjectDrug Resistanceen_US
dc.subjectHif1a-As2en_US
dc.subjectSclcen_US
dc.titleKnockdown of lncRNA HIF1A-AS2 increases drug sensitivity of SCLC cells in association with autophagyen_US
dc.typeArticleen_US

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