Anti-proliferative effects of beta-blocker propranolol on human lung cancer and noncancer cells

dc.contributor.authorTerzi, Menderes Yusuf
dc.contributor.authorUrhan-kucuk, Meral
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) has been recently discovered to possess anti-tumorigenic effects in cancer patients. So, we aimed to enlighten the in vitro effects of PRO in A549 lung cancer cells and BEAS2B nontumoral lung cells.METHODS: The gene expression levels of apoptotic proteins; caspases 3, 8, and 9 (CASP3, 8, 9), apoptosis inducing factor (AIF), and DNA damage inducible transcript 3 (DDIT3) and cell cycle regulatory proteins; WEE1 G2 checkpoint kinase (WEE1) and cyclin dependent kinase inhibitor 1A (CDKN1A) were analyzed with quantitative reverse-transcription PCR to assess the effect of PRO on A549 tumor and BEAS2B nontumoral cells. The protein levels of CASP3 and AIF1 were detected with Western blot.RESULTS: PRO exerted its anti-tumorigenic effects against A549 cells by arresting cell cycle via CDNK1A and by inducing apoptosis via caspase-dependent (CASP3) and -independent pathways (AIF, DDIT3). As to nontumoral BEAS2B cells, PRO decreased the cell viability at a lesser extent compared to tumoral cells. In contrast to tumor cells, PRO reduced the protein levels of CASP3 and AIF1. Notably, at 48th hour of PRO treatment, we observed a sustained expression of elevated DDIT3 mRNA levels at 24h in BEAS2B cells unlike in A549 cells.CONCLUSION: We suggest that D DIT3 and CDKN1A play a critical role during cell fate decision after PRO treatment by protecting nontumoral cells against apoptosis and by triggering apoptosis in tumor cells. The selective action mechanism of PRO with less cytotoxicity in nontumoral lung cells puts it forward as a promising adjuvant agent in lung cancer therapy (Tab. 1, Fig. 4, Ref. 50). Text in PDF www.elis.sken_US
dc.identifier.doi10.4149/BLL_2023_045
dc.identifier.endpage303en_US
dc.identifier.issn0006-9248
dc.identifier.issn1336-0345
dc.identifier.issue4en_US
dc.identifier.pmid36598324en_US
dc.identifier.scopus2-s2.0-85149999724en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage292en_US
dc.identifier.urihttps://doi.org/10.4149/BLL_2023_045
dc.identifier.urihttps://hdl.handle.net/20.500.12483/11862
dc.identifier.volume124en_US
dc.identifier.wosWOS:000957700000008en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherAepress Sroen_US
dc.relation.ispartofBratislava Medical Journal-Bratislavske Lekarske Listyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectpropranololen_US
dc.subjectBEAS2Ben_US
dc.subjectA549en_US
dc.subjectlung canceren_US
dc.subjectapoptosisen_US
dc.subjectDDIT3en_US
dc.titleAnti-proliferative effects of beta-blocker propranolol on human lung cancer and noncancer cellsen_US
dc.typeArticleen_US

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