Sorafenib inhibits the growth of human non-small cell lung cancer cells and induces their apoptosis
Huiwei Qi, Lihong Fan
Abstract
Huiwei Qi, Lihong Fan
Abstract
Objective: To observe the effects of sorafenib on the proliferation and apoptosis of human non-small cell lung cancer (NSCLC) A549 and H1299 cells and to explore their possible mechanisms. Methods: The A549 and H1299 cells were treated with sorafenib at different concentrations. The inhibitory rate of cell proliferation was assessed by cell counting kit-8 (CCK-8). The apoptosis and the cell cycle distribution were analyzed by flow cytometry (FCM). The expression levels of phosphorylated extracellular signal-regulated kinase (p-ERK) and phosphorylated-Akt (p-Akt) proteins in A549 and H1299 cells were examined by Western blotting. Results: The proliferation of A549 and H1299 cells was inhibited via treatment with different concentrations of sorafenib in a dose-dependent manner (P<0.05). Sorafenib can induce apoptosis. The percentage of cells at G0/G1 phase was significantly increased, and which at S phase was significantly decreased in sorafenib-treated group, as compared with those in the control group (P<0.05). The expression level of p-ERK protein in A549 and H1299 cells treated with sorafenib was lower than that in the untreated control group (P<0.05). Conclusion: Sorafenib can inhibit the proliferation of human NSCLC A549 and H1299 cells and induce the apoptosis. This effect may be associated with the block of ERK signaling pathway. DOI:10.3781/j.issn.1000-7431.2011.12.005
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Objective: To observe the effects of sorafenib on the proliferation and apoptosis of human non-small cell lung cancer (NSCLC) A549 and H1299 cells and to explore their possible mechanisms. Methods: The A549 and H1299 cells were treated with sorafenib at different concentrations. The inhibitory rate of cell proliferation was assessed by cell counting kit-8 (CCK-8). The apoptosis and the cell cycle distribution were analyzed by flow cytometry (FCM). The expression levels of phosphorylated extracellular signal-regulated kinase (p-ERK) and phosphorylated-Akt (p-Akt) proteins in A549 and H1299 cells were examined by Western blotting. Results: The proliferation of A549 and H1299 cells was inhibited via treatment with different concentrations of sorafenib in a dose-dependent manner (P<0.05). Sorafenib can induce apoptosis. The percentage of cells at G0/G1 phase was significantly increased, and which at S phase was significantly decreased in sorafenib-treated group, as compared with those in the control group (P<0.05). The expression level of p-ERK protein in A549 and H1299 cells treated with sorafenib was lower than that in the untreated control group (P<0.05). Conclusion: Sorafenib can inhibit the proliferation of human NSCLC A549 and H1299 cells and induce the apoptosis. This effect may be associated with the block of ERK signaling pathway. DOI:10.3781/j.issn.1000-7431.2011.12.005
Key concepts: Sorafenib, Apoptosis, A549 cell, Protein kinase B, MAPK/ERK pathway, Cell growth, Cell cycle, Flow cytometry