Antineoplastic effects of erufosine on small cell and non-small cell lung cancer cells through induction of apoptosis and cell cycle arrest

dc.authorscopusid57202859815
dc.contributor.authorAbdik, Huseyin
dc.contributor.authorAbdik, Hüseyin
dc.date.accessioned2022-03-04T19:12:25Z
dc.date.available2022-03-04T19:12:25Z
dc.date.issued2022
dc.departmentİZÜ
dc.description.abstractBackground Lung cancer (LC) is the most common types of cancer worldwide and is marked by high mortality rate. LC is classified into two major types due to their molecular and histological properties; non-small cell lung cancer (NSCLC) A549 and small cell lung cancer (SCLC). Currently, surgery, chemotherapy and radiation therapy are the most common treatment options of LC. However, the survival rate of LC is still very poor. Therefore, new treatment strategies are urgently needed. Erufosine (ErPC3) is a novel alkylphosphocholine and inhibits the translocation of Akt to the plasma membrane. Methods and results In the current study, the effects of ErPC3 in NSCLC cell line A549 and SCLC cell line DMS 114 in terms of cell viability, induction of apoptosis, cell cycle phase distribution, gene and protein expression levels, and migration capacity were investigated. 25 mu M ErPC3 exhibited dose-dependent cytotoxicity against in both cancer cells. However, DMS 114 was more sensitive to ErPC3 than A549. Similarly, ErPC3 induced apoptotic cell ratio in DMS114 was significantly greater than A549. 25 mu M ErPC3 caused the accumulation of both cell in G2/M phase. The levels of BCL-2 were downregulated and CASPASE 3-7 and BAX were upregulated while p-Akt levels were reduced in A549 and DMS 114 cells treated with 25 mu M ErPC3. Besides, ErPC3 displayed anti-migratory effect on A549 and DMS 114. Conclusion These findings suggest that ErPC3 may be a promising novel therapeutic candidate for treatment of LC. ErPC3 treatment merits further investigation as potential agent against LC.
dc.description.sponsorshipYeditepe University
dc.description.sponsorshipThis study was funded by Yeditepe University. The author thanks to Prof. Fikrettin Sahin for providing laboratory facilities and Prof. Ferda Kaleagasoglu and Prof. Martin Berger for providing Erufosine.
dc.identifier.doi10.1007/s11033-022-07117-6
dc.identifier.issn0301-4851
dc.identifier.issn1573-4978
dc.identifier.pmid35015224
dc.identifier.scopus2-s2.0-85122679320
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1007/s11033-022-07117-6
dc.identifier.urihttps://hdl.handle.net/20.500.12436/3192
dc.identifier.wosWOS:000741242600001
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorAbdik, Hüseyin
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofMolecular Biology Reports
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectLung cancer cells
dc.subjectErufosine
dc.subjectAntineoplastic agent
dc.subjectApoptosis
dc.subjectAKT
dc.subjectAKT
dc.subjectALKYLPHOSPHOCHOLINE
dc.subjectPATHWAY
dc.subjectEXPRESSION
dc.subjectERUCYLPHOSPHOHOMOCHOLINE
dc.subjectEPIDEMIOLOGY
dc.subjectPROGRESSION
dc.subjectINHIBITION
dc.subjectSURVIVAL
dc.subjectETIOLOGY
dc.titleAntineoplastic effects of erufosine on small cell and non-small cell lung cancer cells through induction of apoptosis and cell cycle arrest
dc.typeArticle
dspace.entity.typePublication
relation.isAuthorOfPublication0314d598-3ca7-4184-b508-6420ea4bf7a3
relation.isAuthorOfPublication.latestForDiscovery0314d598-3ca7-4184-b508-6420ea4bf7a3

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