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[目的]探讨凝血酶恶性转化人支气管上皮细胞时丝裂原激活蛋白激酶(p44/42MAPK)信号通路活化状态。[方法]逆转录—聚合酶链反应(RT-PCR)检测凝血酶受体在BEP2D细胞的表达水平及凝血酶刺激后原癌基因c-fos、c-myc转录表达情况。用免疫印迹法(Western blot)检测不同浓度凝血酶刺激后不同时间p44/42MAPK磷酸化状态。[结果]凝血酶受体PAR1、PAR3、PAR4在BEP2D细胞均有表达。凝血酶刺激后出现p44/42MAPK激活。相应地,c-fos、c-myc基因转录上调。[结论]凝血酶与其受体结合后可激活p44/42MAPK信号转导通路,原癌基因转录扩增导致BEP2D细胞基因组不稳定性增加,细胞出现癌变。
[Objective] To investigate the activation of p44 / 42 MAPK signaling pathway in thrombin-induced malignant transformation of human bronchial epithelial cells. [Method] Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to detect the expression level of thrombin receptor in BEP2D cells and the transcriptional expression of c-fos and c-myc genes after thrombin stimulation. Western blotting was used to detect the phosphorylation of p44 / 42MAPK at different times after stimulation with different concentrations of thrombin. [Results] The thrombin receptors PAR1, PAR3 and PAR4 were all expressed in BEP2D cells. Thrombin stimulation p44 / 42MAPK activation. Accordingly, c-fos, c-myc gene transcription is up-regulated. [Conclusion] Thrombin can activate p44 / 42 MAPK signal transduction pathway when it binds to its receptor. Transcriptional amplification of protooncogene leads to increased genomic instability and carcinogenesis in BEP2D cells.