Flow cytometry and gene expression modulation by euphorbia rigida Methanol extract in A549 lung cancer cells: Induction of apoptosis through bax, caspase-9, and bcl-2 pathways
| dc.contributor.author | Sarı, Zeynep Betül | |
| dc.contributor.author | Sarı, Muhammet Emin | |
| dc.contributor.author | Aytar, Erdi Can | |
| dc.contributor.author | Gümrükçüoğlu, Abidin | |
| dc.contributor.author | İncilay Torunoğlu, Emine | |
| dc.contributor.author | Özdemir Sancı, Tuba | |
| dc.contributor.author | Demirel, Gamze | |
| dc.contributor.author | Durmaz, Alper | |
| dc.date.accessioned | 2025-06-17T05:31:17Z | |
| dc.date.available | 2025-06-17T05:31:17Z | |
| dc.date.issued | 2025 | |
| dc.department | AÇÜ | |
| dc.description.abstract | Non-small cell lung cancer (NSCLC) remains a major cause of cancer-related mortality. This study investigates the cytotoxic effects of Euphorbia rigida extract on A549 NSCLC cells and its potential as a therapeutic agent. Cellular morphology was observed microscopically, and cell viability was evaluated using dose-dependent proliferation assays. Apoptosis-related gene expression—including Bax, Bcl-2, and Caspase-9—was analyzed via quantitative PCR (qPCR). Chromatographic methods identified bioactive flavonoids, and molecular docking assessed their binding to cancer-related proteins. Additionally, absorption, distribution, metabolism, excretion, and toxicity (ADMET) profiles were evaluated. The extract induced apoptotic morphological changes such as cell shrinkage and loss of intercellular contact. A dose-dependent reduction in A549 viability was observed, with an IC50 of 0.5 mg mL−1. Gene expression indicated activation of the intrinsic mitochondrial apoptotic pathway, with increased Bax and Caspase-9 and decreased Bcl-2 expression. Flow cytometry using Annexin V-allophycocyanin (V-APC) staining revealed selective cytotoxicity: significant apoptosis in A549 cells while preserving viability in BEAS-2B normal lung epithelial cells. Identified flavonoids included quercetin, apigenin, and myricetin, which showed strong binding affinities in docking studies. ADMET profiling supported their drug-likeness. These findings highlight E. rigida potential in NSCLC treatment via apoptosis induction and selective cytotoxicity. | |
| dc.identifier.doi | 10.1002/adbi.202500136 | |
| dc.identifier.issn | 27010198 | |
| dc.identifier.pmid | 40432491 | |
| dc.identifier.scopus | 2-s2.0-105006688448 | |
| dc.identifier.scopusquality | Q2 | |
| dc.identifier.uri | https://hdl.handle.net/11494/5525 | |
| dc.identifier.wos | WOS:001497264300001 | |
| dc.identifier.wosquality | Q3 | |
| dc.indekslendigikaynak | Scopus | |
| dc.indekslendigikaynak | Web of Science | |
| dc.indekslendigikaynak | PubMed | |
| dc.institutionauthor | Gümrükçüoğlu, Abidin | |
| dc.institutionauthor | Durmaz, Alper | |
| dc.language.iso | en | |
| dc.publisher | John Wiley and Sons Inc | |
| dc.relation.ispartof | Advanced Biology | |
| dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | |
| dc.rights | info:eu-repo/semantics/embargoedAccess | |
| dc.subject | A549 cells | |
| dc.subject | Bax | |
| dc.subject | Bcl-2 | |
| dc.subject | BEAS-2B | |
| dc.subject | Caspase-9 | |
| dc.subject | Cytotoxicity | |
| dc.subject | Euphorbia rigida | |
| dc.subject | Molecular docking | |
| dc.title | Flow cytometry and gene expression modulation by euphorbia rigida Methanol extract in A549 lung cancer cells: Induction of apoptosis through bax, caspase-9, and bcl-2 pathways | |
| dc.type | Article |
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