Propranolol Treatment Reduces A549-Derived Lung Cancer Spheroids via Intrinsic Apoptosis

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dc.contributor.authorTerzi, Menderes Yusuf
dc.date.accessioned2024-09-18T20:55:29Z
dc.date.available2024-09-18T20:55:29Z
dc.date.issued2023
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractObjective: Propranolol (PRO), a non-selective beta-adrenergic receptor inhibitor, has been recently discovered to possess anti-tumorigenic effects in cancer patients. Therefore, we aimed to investigate the in vitro effects of PRO in A549-derived lung cancer spheroids in terms of cell viability, spheroid formation, cell cycle regulation, cell differentiation, and apoptosis. Materials and Methods: The effect of 24-hour PRO treatment on A549 cell viability was assessed using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. A sub-cytotoxic PRO concentration (125 mu M) was employed to evaluate its impact on the clonogenicity of A549-derived cancer spheroids after seven days of incubation. Messenger Ribonucleic Acid (mRNA) levels of cell cycle regulators including cyclin-dependent kinase inhibitor 1A (p21) and G2 checkpoint kinase (WEE1), apoptotic markers such as caspases 3, 8, 9 (CASP3, CASP8, CASP9), and stem cell differentiation markers, namely POU class 5 homeobox 1 (octamer-binding transcription factor 4 (OCT4)), prominin 1 (CD133), and adenosine triphosphate (ATP) binding cassette subfamily G member 2 (ABCG2) were measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR) after a 24-hour treatment of cancer spheroids with PRO. Results: PRO treatment reduced cell viability and inhibited the clonogenicity of cancer spheroids by activating intrinsic apoptotic markers CASP3 and CASP9, leading to cell cycle arrest via increased p21 expression. PRO did not significantly alter stem cell differentiation markers. Conclusion: The proliferation and clonogenic activity of lung cancer spheroids can be effectively suppressed with PRO, primarily through inducing intrinsic apoptosis following p21-mediated cell cycle arrest. While short-term PRO exposure did not affect the gene expression levels of stem cell differentiation markers, the notable decrease in both cell viability and spheroid formation efficiency suggests the potential of PRO as a therapeutic drug in lung cancer treatment.en_US
dc.identifier.doi10.14744/cpr.2023.37929
dc.identifier.endpage623en_US
dc.identifier.issn2980-2156
dc.identifier.issue6en_US
dc.identifier.startpage614en_US
dc.identifier.trdizinid1252013en_US
dc.identifier.urihttps://doi.org/10.14744/cpr.2023.37929
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay/1252013
dc.identifier.urihttps://hdl.handle.net/20.500.12483/11861
dc.identifier.volume45en_US
dc.identifier.wosWOS:001118613800001en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakTR-Dizinen_US
dc.language.isoenen_US
dc.publisherErciyes Univ Sch Medicineen_US
dc.relation.ispartofJournal of Clinical Practice and Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectPropranololen_US
dc.subjectA549 spheroiden_US
dc.subjectlung canceren_US
dc.subjectapoptosisen_US
dc.subjectcell differentiation.en_US
dc.titlePropranolol Treatment Reduces A549-Derived Lung Cancer Spheroids via Intrinsic Apoptosisen_US
dc.typeArticleen_US

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