Piceatannol induces apoptotic cell death through activation of caspase-dependent pathway and upregulation of ROS-mediated mitochondrial dysfunction in pancreatic cancer cells

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dc.contributor.authorAyan, Ilknur Cinar
dc.contributor.authorGuclu, Ebru
dc.contributor.authorVural, Hasibe
dc.contributor.authorDursun, Hatice Gul
dc.date.accessioned2024-02-23T13:59:23Z
dc.date.available2024-02-23T13:59:23Z
dc.date.issued2022
dc.departmentNEÜen_US
dc.description.abstractBackground Piceatannol is a naturally occurring plant-derived phenolic compound (stilbenoid), an analogue of resveratrol. It has been shown that, piceatannol has biological activity properties such as antiproliferative, antioxidative, anti-inflammatory and proapoptotic, in various human cancer studies in vitro and in vivo. Objectives and methods In this study, it was aimed to investigate whether piceatannol induces apoptosis through anticancer activity methods (cell viability, colony formation, annexin-V/7-AAD, ROS (Reactive oxygen species), MMP (Mitochondrial membrane potential), wound healing, invasion assay, RT-qPCR (Real-Time Quantitative Polymerase Chain Reaction), western blotting in PANC-1 and MIA PaCa-2 pancreatic cancer (PC) cell lines. Results According to our results, piceatannol decreased cell viability in a dose and time-dependent manner [the half-maximal inhibitory concentration (IC50): 60 mu M in PANC-1 and IC50: 90 mu M in MIA PaCa-2 cell line at 48 h (h)] and caused significant changes in the expression of apoptosis-related genes and protein. Piceatannol induced apoptosis in PANC-1 and MIA PaCa-2 cells, accompanied by increased ROS production, decreased MMP, and increased Caspase-3-9 activity. Piceatannol also inhibited colony-forming abilities, invasion, and migration of PC cells. Conclusion Our results show that piceatannol has an anti-cancerogenic effect on PANC-1 and MIA PaCa-2 cells, and exerts this effect by suppressing proliferation and inducing apoptosis. Therefore, piceatannol could be considered to be a potential chemotherapeutic agent candidate for the treatment and prevention of PC. [GRAPHICS] .en_US
dc.identifier.doi10.1007/s11033-022-08006-8
dc.identifier.endpage11957en_US
dc.identifier.issn0301-4851
dc.identifier.issn1573-4978
dc.identifier.issue12en_US
dc.identifier.pmid36260179en_US
dc.identifier.scopus2-s2.0-85140133508en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage11947en_US
dc.identifier.urihttps://doi.org/10.1007/s11033-022-08006-8
dc.identifier.urihttps://hdl.handle.net/20.500.12452/11164
dc.identifier.volume49en_US
dc.identifier.wosWOS:000870115700001en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofMolecular Biology Reportsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectPiceatannolen_US
dc.subjectPancreatic Cancer Cellsen_US
dc.subjectApoptosisen_US
dc.subjectAnticancer Agentsen_US
dc.subjectPhenolic Compounden_US
dc.subjectResveratrol-Analogueen_US
dc.titlePiceatannol induces apoptotic cell death through activation of caspase-dependent pathway and upregulation of ROS-mediated mitochondrial dysfunction in pancreatic cancer cellsen_US
dc.typeArticleen_US

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