INVESTIGATION OF ANTICANCER MECHANISMS OF A CHALCONE/XANTHINE HYBRID IN NON-SMALL CELL LUNG CANCER | ||
| Bulletin of Pharmaceutical Sciences Assiut University | ||
| Volume 47, Issue 2, December 2024, Pages 1353-1366 PDF (887.13 K) | ||
| Document Type: Original Article | ||
| DOI: 10.21608/bfsa.2024.305647.2224 | ||
| Authors | ||
| Omar Mahmoud Elrehany* 1; Al - Shaimaa Faissal Ahmed2; Hesham A. Abou-Zied3; Alaa M. Hayallah4, 5; Mohamed Abdel-Aziz6; Maiiada Hassan Nazmy1 | ||
| 1Department of Biochemistry, Faculty of pharmacy, Minia University, Minya, Egypt | ||
| 2Department of Pharmacology and Toxicology, Faculty of Pharmacy, Minia University | ||
| 3Medicinal Chemistry Department, Faculty of Pharmacy, Deraya University, Minia, Egypt | ||
| 4Pharmaceutical Organic Chemistry Department, Faculty of Pharmacy, Assiut University, Assiut 71526, Assiut, Egypt | ||
| 5Pharmaceutical Chemistry Department, Faculty of Pharmacy, Sphinx University, New Assiut, Egypt | ||
| 6Medicinal Chemistry Department, Faculty of Pharmacy, Minia University, Minia, Egypt | ||
| Abstract | ||
| Despite major advances in therapy, Lung cancer remains the major cause of death among cancer cases. Chalcone/xanthine Hybrid is a synthetic xanthine derivative that was found to exert an anticancer action in various cancer types. Thus, the current study sought to discover if the chalcone/xanthine hybrid influences the etiology of non-small cell lung cancer (NSCLC). We found that the chalcone/xanthine hybrid inhibited cell cycle progression while inducing apoptosis and causing arrest of the cell cycle in HOP-92 cells. Flow cytometry demonstrated that chalcone/xanthine hybrid strongly induced apoptosis in HOP-92 cells, as well as alterations in apoptosis-related protein expression, including an increase in Bax, caspase3, caspase8, caspase-9, P53 expression, as well as a decrease in Bcl-2 expression. Moreover, the chalcone/xanthine hybrid slowed cell cycle progression from the G1 phase to the S phase. Furthermore, the ratio of phosphorylated proteins (AKT, MEK, ERK½, and P38) to total protein quantity reduced, indicating regulation of downstream protein signaling pathways governing cell cycle growth. Overall, this chalcone/xanthine hybrid may be considered a therapeutic option for NSCLC via apoptosis induction. | ||
| Keywords | ||
| NSCLC (non-small cell lung cancer); HOP-92 (Hopkins-92); MAPK (mitogen activated protein kinase) | ||
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