Inhibitory effect of shikonin on proliferation of lung adenocarcinoma A549 cells
Rui Zhuang-hu
Abstract
Rui Zhuang-hu
Abstract
Objective To investigate the effect of shikonin on proliferation of human lung adenocarcinoma A549 cells and related mechanisms.Methods A549 cells were incubated with shikonin at different concentration(0.5,1,2 and 4 μg/ml) for 0,12,24 and 48 h.Cell proliferation was measured by CCK-8 assay; cell cycle was examined by flow cytometry using propidium iodide staining; and the expressions of pAkt was tested by Western blot assay.Results The viabilities of A549 cells were significantly inhibited after shikonin treatment.Shikonin can induce A549 cells apoptosis,and blocked the cells developing from G1 phase to S phase.The expression of pAkt was markedly decreased after shikonin treatment for 48 h.Conclusion Shikonin inhibits the growth of A549 cells significantly,which may be associated with inhibition of PI3K/Akt signaling pathway.
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Objective To investigate the effect of shikonin on proliferation of human lung adenocarcinoma A549 cells and related mechanisms.Methods A549 cells were incubated with shikonin at different concentration(0.5,1,2 and 4 μg/ml) for 0,12,24 and 48 h.Cell proliferation was measured by CCK-8 assay; cell cycle was examined by flow cytometry using propidium iodide staining; and the expressions of pAkt was tested by Western blot assay.Results The viabilities of A549 cells were significantly inhibited after shikonin treatment.Shikonin can induce A549 cells apoptosis,and blocked the cells developing from G1 phase to S phase.The expression of pAkt was markedly decreased after shikonin treatment for 48 h.Conclusion Shikonin inhibits the growth of A549 cells significantly,which may be associated with inhibition of PI3K/Akt signaling pathway.
Key concepts: A549 cell, Propidium iodide, Apoptosis, Flow cytometry, Cell growth, Cell cycle, Protein kinase B, PI3K/AKT/mTOR pathway