Inhibitory Effect of Epidermal Growth Factor on the Proliferation of Lung Cancer Cell Lines

Seunghee Lee, Hong-Gyun Wu
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引用次数: 1

Abstract

Purpose: Epidermal growth factor (EGF) is known to cause cellular proliferation, differentiation and survival. However, there are a few articles that have reported on the cell killing effect of EGF. We evaluated the effects of EGF on the survival of some lung cancer cell lines and we tried to determine the mechanism of action. Materials and Methods: We examined various lung cancer cell lines. The cultured cells were exposed to radiation alone (0, 2, 5, and 10 Gy), EGF alone (0 ∼1,000 nM) or a combination of radiation and EGF (10 nM). Survival was measured using a clonogenic assay and the expressions of epidermal growth factor receptor (EGFR), Ki-67 and cleavedPARP were detected by western blot analysis. K-ras mutations were detected using polymerase chain reaction and sequencing. Results: Treatment of EGF induced cell death in the lung cancer cell lines. The addition of EGF (10 nM) to radiation (0, 2, 5, and 10 Gy) resulted in an increased cell killing effect of radiation. The EGFR expression decreased with the addition of EGF. EGF increased the expression of cleaved-PARP, but it did not increase the expression of Ki-67. The effects of EGF were not correlated with EGFR mutation or K-ras mutation. Conclusion: In our study, EGF inhibited the proliferation of lung cancer cell lines and it induced apoptosis. EGF enhanced the radiosensitivity of lung cancer cells when EGF was combined with radiation. It is suggested that EGF seem to be one of the cytotoxic agents for lung cancer cell lines. (J Lung Cancer 2010;9(2):64 �� 71)
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表皮生长因子对肺癌细胞系增殖的抑制作用
目的:表皮生长因子(EGF)是引起细胞增殖、分化和存活的重要因子。然而,有一些文章报道了EGF的细胞杀伤作用。我们评估了EGF对一些肺癌细胞系存活的影响,并试图确定其作用机制。材料和方法:我们检测了多种肺癌细胞系。将培养的细胞单独暴露于辐射(0、2、5和10 Gy)、单独暴露于EGF (0 ~ 1,000 nM)或辐射和EGF联合暴露(10 nM)。用克隆法测定存活,用western blot法检测表皮生长因子受体(EGFR)、Ki-67和cleedparp的表达。采用聚合酶链反应和测序检测K-ras突变。结果:EGF可诱导肺癌细胞系细胞死亡。在辐射(0、2、5和10 Gy)中添加EGF (10 nM)可增强辐射对细胞的杀伤作用。EGFR的表达随EGF的加入而降低。EGF增加了cleaved-PARP的表达,但没有增加Ki-67的表达。EGF的作用与EGFR突变或K-ras突变无关。结论:EGF能抑制肺癌细胞株的增殖,诱导细胞凋亡。EGF联合放疗可增强肺癌细胞的放射敏感性。提示EGF可能是肺癌细胞系的细胞毒性因子之一。[J] .肺癌杂志;2010;9(2):64 - 71。
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