阿司匹林通过诱导JNK表达促进其磷酸化抑制肺癌PC14细胞增殖

目的:观察阿司匹林对肺癌PC14细胞的作用及其可能机制。方法:用0,4,8,16 mmol·L^-1阿司匹林处理PC14细胞24,48,72 h,用MTT法和流式细胞术检测细胞增殖及凋亡。为研究其与c-Jun氨基末端激酶(JNK)活化间的关系,先以5μmol·L^-1 SP600125(JNK抑制剂)预处理PC14细胞30 min,加入上述浓度药物继续培养24,48,72 h,检测细胞增殖情况;Western blot检测阿司匹林对JNK活化的影响。结果:MTT结果显示阿司匹林抑制肺癌PC14细胞增殖,同时阿司匹林可引起细胞G0~G1阻滞;阿司匹林通过活化JNK诱导其表达抑制PC14增殖。结论:阿司匹林可抑制PC14细胞增殖,其机制可能与其增强JNK活化及表达有关,这为阿司匹林在肺癌治疗中的进一步应用提供了理论依据。

Aspirin inhibition of proliferation of lung cancer PC14 cells by inducing JNK expression and promoting its phosphorylation

OBJECTIVE To investigate the effect of aspirin on lung cancer PC14 cells and its possible mechanism. METHODS PC14 cells were treated with 0, 4, 8 and 16 mmol·L^-1 aspirin for 24, 48, 72 h. The cells proliferation was measured by MTT and the apoptosis was detected by flow cytometry. In order to study the relationship between PC14 cells proliferation and c-Jun N-terminal Kinase(JNK) activation, PC14 cells were pretreated with 5 μmol·L^-1 SP600125 (JNK inhibitor) for 30 min, and then cultured for 24 h, 48 h and 72 h in the presence of the drugs at the above concentrations to detect cell proliferation. The effect of Aspirin on the activation of JNK was detected by Western blot.RESULTS The results of MTT showed that aspirin inhibited the proliferation of PC14 cells in lung cancer, meanwhile, aspirin could induce G0-G1 arrest in lung cancer cells. Aspirin inhibits PC14 proliferation by activating JNK and inducing its expression. CONCLUSION Aspirin can inhibit the proliferation of PC14 cells, which may be related to the enhancement of JNK activation and expression, which provides a theoretical basis for the potential application of aspirin in the treatment of lung cancer.