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钱越, 戴红良, 李红玉. 低浓度阿司匹林通过活化ERK促进肺癌PC14细胞增殖[J]. 肿瘤防治研究, 2017, 44(12): 787-791. DOI: 10.3971/j.issn.1000-8578.2017.17.0671
引用本文: 钱越, 戴红良, 李红玉. 低浓度阿司匹林通过活化ERK促进肺癌PC14细胞增殖[J]. 肿瘤防治研究, 2017, 44(12): 787-791. DOI: 10.3971/j.issn.1000-8578.2017.17.0671
QIAN Yue, DAI Hongliang, LI Hongyu. Low Concentration of Aspirin Promotes Growth of Human Lung Cancer PC14 Cells Through Activating ERK Signaling[J]. Cancer Research on Prevention and Treatment, 2017, 44(12): 787-791. DOI: 10.3971/j.issn.1000-8578.2017.17.0671
Citation: QIAN Yue, DAI Hongliang, LI Hongyu. Low Concentration of Aspirin Promotes Growth of Human Lung Cancer PC14 Cells Through Activating ERK Signaling[J]. Cancer Research on Prevention and Treatment, 2017, 44(12): 787-791. DOI: 10.3971/j.issn.1000-8578.2017.17.0671

低浓度阿司匹林通过活化ERK促进肺癌PC14细胞增殖

Low Concentration of Aspirin Promotes Growth of Human Lung Cancer PC14 Cells Through Activating ERK Signaling

  • 摘要:
    目的 观察阿司匹林对人肺癌细胞PC14增殖的影响并探讨其作用机制。
    方法 以0、1、2、4、8、16 mmol/L阿司匹林处理肺癌PC14和A549细胞,48 h后以MTT法及集落形成实验检测细胞增殖。为检测低浓度阿司匹林对肺癌PC14细胞增殖的影响与ERK活化间的关系,先以10 μmol/L PD98059(ERK抑制剂)预处理PC14细胞30 min,随后加入不同浓度阿司匹林继续培养48 h或7 d,以MTT法及集落形成实验检测细胞增殖情况,并以蛋白质免疫印迹法检测低浓度阿司匹林对ERK活化的影响。
    结果 低浓度的阿司匹林可以促进肺癌PC14细胞和A549细胞的增殖并明显增强PC14细胞ERK的活化;而PD98059预处理组能明显地抑制阿司匹林诱导的PC14细胞的增殖和存活。
    结论 低浓度阿司匹林可促进人肺癌PC14细胞增殖,其机制可能与其增强ERK活化有关。

     

    Abstract:
    Objective To investigate the effect of aspirin on the proliferation of human lung cancer PC14 cells and explore the underlying mechanisms.
    Methods PC14 cells and A549 cells were treated with 0, 1, 2, 4, 8, and 16 mmol/L aspirin for 48 h, and cell proliferation was examined by MTT and colony formation assay. In order to explore the relationship between the proliferation-enhancing effect of low-dose aspirin and ERK activation, PC14 cells were pretreated with 10μmol/L PD98059 (a specific inhibitor of ERK) for 30 min, and then stimulated by different concentrations of aspirin for 48 h or 7 d, and cell proliferation was tested by MTT and colony formation assay. Western blot was employed to examine the effect of aspirin on ERK activation.
    Results Aspirin at low concentration promoted human lung cancer PC14 and A549 cells growth and induced ERK activation in PC14 cells. PD98059 pretreatment significantly inhibited aspirin-induced proliferation of PC14 cells.
    Conclusion Low concentration of aspirin could promote the growth of human lung cancer PC14 cells, which may be related to the activation of ERK.

     

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