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- 저자 : Dalia D. Abd El‑Monem (검색결과 1 건)
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Graviola leaves extract enhances the anticancer effect of cisplatin on various cancer cell lines
Mai G. Awad,Ramadan A. Ali,Dalia D. Abd El‑Monem,Mohammed A. El‑Magd 대한독성 유전단백체 학회 2020 Molecular & cellular toxicology Vol.16 No.4
Background Cisplatin (CIS) is widely applied as an anticancer drug for various cancer types, including liver, breast, colorectal, and pancreatic cancers; however, its usage is limited due to side efects. Objective We investigated whether combined therapy of Graviola (Annona muricata) leaves extract (GLE) and CIS could reduce CIS doses without decreasing its anticancer potential. Methods The MCF7, HepG2, CaCo2, or PANC1 cells were divided into four groups for each cell line as follows: group1 (G1): untreated cells, G2: cells treated with GLE, G3: cells treated with CIS, and G4: cells treated with GLE, after 2 h treated with CIS. All combinations were prepared as non-constant ratio from GLE. The cytotoxicity, gene expression, cell cycle arrest were determined by MTT assay, real-time PCR, and cell fow cytometry, respectively. Results Treatment with GLE and/or CIS-induced cytotoxic efect on HepG2, MCF7, CaCo2, and PANC1 cancer cells with the best efect of combined therapy. All twelve non-constant ratio combinations (GLE+CIS) for each cell line resulted in a signifcant higher cytotoxic efect than single drug treatment. The combination index (CI) values for all combinations were less than one, indicating the presence of synergistic cytotoxic efect between CIS and GLE against the four cancer cell lines. This anticancer efect was triggered through mitochondrial-dependent apoptosis with the downregulation of caspase3, Bax, and p53 and upregulation of Bcl2. GLE also shifted G0/G1 phase of cell cycle arrest induced by CIS to S and G2/M phases. Interestingly, this combined therapy did not afect oxidative stress (indicated by higher malondialdehyde level and lower activities of SOD, CAT, and GPX) induced by CIS; however, it downregulated the expression of MAPK1 and multidrug resistance gene MDR1.
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