CAJ | 학술논문

目的：探讨Fas信号通路促进胃癌细胞侵袭转移的可能相关机制。方法以低浓度FasL处理胃癌细胞株AGS，免疫印迹及ELISA检测上皮间质转化（epithelial-mesenehymal transition, EMT）的分子生物学标记改变；稳定沉默Snail及Twist转录因子，transwell小室侵袭实验检测FasL处理后胃癌细胞的侵袭能力；免疫印迹检测信号通路激活状态及相应的抑制效应。结果 FasL可以诱导AGS细胞株出现EMT表型，并可促进胃癌细胞的侵袭转移能力。同时该过程中出现ERK1/2信号通路的激活，而抑制ERK1/2信号通路，可以抑制FasL诱导EMT及提高肿瘤侵袭能力的作用。胃癌组织中相应分子生物学标记的表达变化符合EMT的发生。结论 Fas信号通路能够激活ERK1/2通路诱导EMT的发生，并且能通过该机制增强胃癌细胞AGS的活动能力。
목적：탐토Fas신호통로촉진위암세포침습전이적가능상관궤제。방법이저농도FasL처리위암세포주AGS，면역인적급ELISA검측상피간질전화（epithelial-mesenehymal transition, EMT）적분자생물학표기개변；은정침묵Snail급Twist전록인자，transwell소실침습실험검측FasL처리후위암세포적침습능력；면역인적검측신호통로격활상태급상응적억제효응。결과 FasL가이유도AGS세포주출현EMT표형，병가촉진위암세포적침습전이능력。동시해과정중출현ERK1/2신호통로적격활，이억제ERK1/2신호통로，가이억제FasL유도EMT급제고종류침습능력적작용。위암조직중상응분자생물학표기적표체변화부합EMT적발생。결론 Fas신호통로능구격활ERK1/2통로유도EMT적발생，병차능통과해궤제증강위암세포AGS적활동능력。
Objective To explore the possible mechanisms of the metastasis promotion induced by Fas signaling pathway in gastric cancer. Methods Gastric cancer cell line AGS was treated with low-dose FasL and the alteration of EMT (epithelial-mesenehymal transition) biology markers were detected by immunoblot and enzyme linked immunosorbent assay,respectively. Two transcription factors Snail and Twist were stablely knocked-down, and transwell chamber migration assay was performed to measure the motility of the pretreated gastric cancer cells. Immunoblot was used to assess the activations and the motility changes of AGS after pre-treated with inhibitor of relative pathways during the procedure. Results FasL induced the occurrence of EMT in AGS cell line, which might contribute to the motility and metastasis of gastric cancer cells. In the process of EMT, ERK1/2 signaling pathway was activated and the suppression of this pathway inhibited the Fas induced EMT and improved the migration ability of gastric cancer cells. The expression variation of relevant biology markers in gastric cancer tissues was correspond to EMT occurrence. Conclusion Fas signaling pathway can promote the metastasis of AGS cell line through EMT with the activation of ERK1/2 pathway.