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Published:
Mar 18, 2019Keywords:
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Main Article Content
7-Piperazine ethyl chrysin inhibits proliferation of lung cancer cells via induction of apoptosis
Abstract
Purpose: To investigate the effect of 7-piperazine ethyl chrysin (PEC) on A-427 and A-549 lung cancer cell lines.
Methods: The cell lines were incubated with PEC at doses of 2, 4, 6, 8 and 10 μM for 24, 48 and 72 h, and their viabilities at each time interval were assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay. Cell apoptosis was evaluated with annexin V fluorescein isothiocyanate/propidium iodide staining, while the expression of ERK1/2 protein was determined using western blot. The involvement of ERK1/2 in the effect of PEC on viability and apoptosis was assessed by incubating the cells with PD98059 (an inhibitor of ERK1/2).
Results: Exposure to PEC at doses ≥ 4 μM significantly reduced the viability of A-427 and A-549 cell lines in time- and concentration-dependent manners at 48 h (p < 0.02). The viability of A-427 and A-549 cells was reduced to 21 and 18 %, respectively, on treatment with 8 μM PEC for 48 h. Moreover, PEC treatment induced apoptosis in A-427 (59.67 %) and A-549 (61.37 %) cells after 48 h. Western blot data revealed that PEC also significantly inhibited phosphorylation of ERK1/2 in both cancer cell lines (p < 0.05). Incubation of A-427 and A-549 cells with PD98059 for 48 h also reduced their viability and induced their apoptosis (p < 0.05).
Conclusion: These results indicate that PEC inhibits the viability of lung cancer cells via inhibition of ERK1/2 expression. Thus, PEC may be efective for the treatment of lung carcinoma but further studies
are required to ascertain this.
Keywords: 7-Piperazine ethyl chrysin, Lung cancer cells, Apoptosis, Viability, inhibition
