现代消化及介入诊疗
現代消化及介入診療
현대소화급개입진료
MODERN DIGESTION & INTERVENTION
2013年
4期
208-211
,共4页
石萌%李文静%王亚东%郑浩轩
石萌%李文靜%王亞東%鄭浩軒
석맹%리문정%왕아동%정호헌
Fas信号%非凋亡作用%剂量依赖性%侵袭转移
Fas信號%非凋亡作用%劑量依賴性%侵襲轉移
Fas신호%비조망작용%제량의뢰성%침습전이
Fas signalling%Non-apoptotic ability%Dose-dependent%Invasion and metastasis
目的探讨Fas通路的非凋亡信号在胃癌细胞株AGS中促进增殖转移的作用。方法流式细胞仪检测AGS细胞表面Fas及FasL表达情况;根据FasL不同作用浓度梯度,绘制细胞生长曲线;shRNA沉默AGS的Fas表达后,或NOK-1拮抗FasL后,利用transwell实验检测AGS的侵袭能力;免疫组化检测FasL表达与E-cadherin关系。结果低浓度的FasL(12.5 ng/ml)刺激对细胞增殖无明显抑制作用,反而能提高肿瘤细胞的侵袭能力。在沉默Fas受体或经NOK-1拮抗FasL后,该效应减弱。FasL和E-cadherin在胃癌组织中的表达呈负性相关。结论低剂量的FasL不能诱导AGS产生凋亡效应,反而通过Fas信号通路促进其侵袭转移能力。
目的探討Fas通路的非凋亡信號在胃癌細胞株AGS中促進增殖轉移的作用。方法流式細胞儀檢測AGS細胞錶麵Fas及FasL錶達情況;根據FasL不同作用濃度梯度,繪製細胞生長麯線;shRNA沉默AGS的Fas錶達後,或NOK-1拮抗FasL後,利用transwell實驗檢測AGS的侵襲能力;免疫組化檢測FasL錶達與E-cadherin關繫。結果低濃度的FasL(12.5 ng/ml)刺激對細胞增殖無明顯抑製作用,反而能提高腫瘤細胞的侵襲能力。在沉默Fas受體或經NOK-1拮抗FasL後,該效應減弱。FasL和E-cadherin在胃癌組織中的錶達呈負性相關。結論低劑量的FasL不能誘導AGS產生凋亡效應,反而通過Fas信號通路促進其侵襲轉移能力。
목적탐토Fas통로적비조망신호재위암세포주AGS중촉진증식전이적작용。방법류식세포의검측AGS세포표면Fas급FasL표체정황;근거FasL불동작용농도제도,회제세포생장곡선;shRNA침묵AGS적Fas표체후,혹NOK-1길항FasL후,이용transwell실험검측AGS적침습능력;면역조화검측FasL표체여E-cadherin관계。결과저농도적FasL(12.5 ng/ml)자격대세포증식무명현억제작용,반이능제고종류세포적침습능력。재침묵Fas수체혹경NOK-1길항FasL후,해효응감약。FasL화E-cadherin재위암조직중적표체정부성상관。결론저제량적FasL불능유도AGS산생조망효응,반이통과Fas신호통로촉진기침습전이능력。
Objective To explore the non-apoptotic ability of Fas signaling pathway to promote the proliferation and the metastasis in gastric cancer cell line AGS. Methods Flow cytometry was used to detect AGS cell surface expression of Fas and FasL expression. According to the different role of FasL concentration gradient, we draw the cell growth curve. Transwell experiments were used to test the AGS invasion ability after silencing AGS Fas expression, or antagonsting the ability with NOK-1. Immunohistochemical assay was used to detcet FasL expression of E-cadherin. Results No significant inhibition and tumor cell invasion was found after low concentration of FasL (12.5 ng/ml) stimulation. In silenced Fas receptor or FasL antagonized by NOK-1 , the effect was weakend. The expression of FasL and E-cadherin in gastric cancer tissues showed a negative correlation. Conclusion Low doses of FasL failed to induce AGS produce apoptotic effects, but through Fas signaling pathway can promote its invasion and metastasis.