Propofol orchestrates long non-coding RNAs in MCF7 cells, unraveling new avenues for breast cancer intervention

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dc.contributor.authorBiray Avci C.
dc.contributor.authorEdgunlu T.G.
dc.contributor.authorSuzek T.
dc.contributor.authorOzates N.P.
dc.contributor.authorGoker Bagca B.
dc.contributor.authorDemirtas Bilgic A.
dc.contributor.authorOzdemir C.
dc.date.accessioned2024-08-31T07:42:26Z
dc.date.available2024-08-31T07:42:26Z
dc.date.issued2024
dc.departmentEge Üniversitesien_US
dc.description.abstractLong non-coding RNAs (lncRNAs) play a dynamic role in gene expression regulation and serve as potential therapeutic targets in breast cancer. The anticancer effect of propofol, an anesthetic agent, has been proven, but its interaction with lncRNAs has not been adequately investigated. This study aims to reveal the interactions between propofol and lncRNAs and contribute to the understanding of its therapeutic potential in the treatment of breast cancer. We evaluated the effects of propofol on cell viability, apoptosis, and mitochondrial membrane potential in MCF7 cells. The study used qRT-PCR to analyze cancer-related lncRNA expressions following propofol treatment; this was supported by RNA-RNA interaction predictions and in silico functional analysis using selected datasets and the R cluster Profiler GSEABase package. Propofol showed a cytotoxic effect at higher doses in MCF7 breast cancer cells, inducing necrosis. Propofol regulated (IGF2-AS, MRPL23-AS1, PANDAR, HULC) and down-regulated (IWT1-AS, HOXA-AS2, H19, GACAT1, MIAT) the expression levels of various lncRNAs in MCF7 cells. Our research revealed complex interactions of MALAT1 lncRNA with both upregulated and downregulated genes. Additionally, three rRNA genes (LSU-rRNA, RNA45SN3, and SSU-rRNA) were identified to interact with both groups of lncRNAs. Propofol potentially targets chemotherapy resistance by regulating UCA1, LINC-RoR1, and MEG3. Wikipathways' pathway enrichment analysis identified two downregulated lncRNAs, UCA1 and LINC-RoR1, and an upregulated MEG3, implicated in lncRNA-mediated chemotherapeutic resistance mechanisms. Our study illuminates the intricate interplay of lncRNAs and their potential contribution to propofol's anti-cancer effects in breast cancer, offering new avenues for therapeutic exploration and advancement. © 2024en_US
dc.description.sponsorshipMugla Sitki Kocman University; Research Foundation Office, (19/085/02/3/4)en_US
dc.identifier.doi10.1016/j.ejmcr.2024.100186
dc.identifier.issn2772-4174
dc.identifier.scopus2-s2.0-85197766126en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.urihttps://doi.org10.1016/j.ejmcr.2024.100186
dc.identifier.urihttps://hdl.handle.net/11454/103878
dc.identifier.volume12en_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherElsevier Masson s.r.l.en_US
dc.relation.ispartofEuropean Journal of Medicinal Chemistry Reportsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.snmz20240831_Uen_US
dc.subjectBreast canceren_US
dc.subjectIn silicoen_US
dc.subjectlncRNAen_US
dc.subjectPropofolen_US
dc.subjectRNA-RNA interactionsen_US
dc.titlePropofol orchestrates long non-coding RNAs in MCF7 cells, unraveling new avenues for breast cancer interventionen_US
dc.typeArticleen_US

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