安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
ACTA UNIVERSITY MEDICINALIS ANHUI
2014年
10期
1379-1381,1382
,共4页
杨彩玲%崔卫刚%张应花%路德荣%刘进忠
楊綵玲%崔衛剛%張應花%路德榮%劉進忠
양채령%최위강%장응화%로덕영%류진충
埃克替尼%涎腺腺样囊性癌细胞%线粒体%凋亡
埃剋替尼%涎腺腺樣囊性癌細胞%線粒體%凋亡
애극체니%연선선양낭성암세포%선립체%조망
icotinib%adenoid cystic carcinoma cell%mitochondrion%apoptosis
目的利用涎腺腺样囊性癌细胞系ACC-M细胞为模型,研究不同浓度埃克替尼( icotinib)对涎腺腺样囊性癌细胞系ACC-M细胞凋亡的影响以及线粒体在 icotinib 诱导ACC-M细胞凋亡中的作用。方法 icotinib 和 P53抑制剂( PFT)分别处理ACC-M细胞,应用噻唑蓝比色法检测细胞活性,利用 Western blot 法检测 P53和胞质内细胞色素 C ( Cyt C)蛋白的表达变化,用Caspase-3凋亡相关蛋白活力检测ACC-M细胞的凋亡情况。结果 icotinib可抑制ACC-M细胞的活性,增加胞质Cyt C蛋白的表达和P53在线粒体的转位并诱导ACC-M细胞凋亡。用PFT预处理后,icotinib诱导ACC-M细胞的凋亡明显下降,线粒体蛋白P53的表达降低,胞质内Cyt C表达减少, Caspase-3凋亡相关蛋白活力下降。结论 icotinib可能通过诱导P53转位到线粒体进而促进ACC-M细胞凋亡。
目的利用涎腺腺樣囊性癌細胞繫ACC-M細胞為模型,研究不同濃度埃剋替尼( icotinib)對涎腺腺樣囊性癌細胞繫ACC-M細胞凋亡的影響以及線粒體在 icotinib 誘導ACC-M細胞凋亡中的作用。方法 icotinib 和 P53抑製劑( PFT)分彆處理ACC-M細胞,應用噻唑藍比色法檢測細胞活性,利用 Western blot 法檢測 P53和胞質內細胞色素 C ( Cyt C)蛋白的錶達變化,用Caspase-3凋亡相關蛋白活力檢測ACC-M細胞的凋亡情況。結果 icotinib可抑製ACC-M細胞的活性,增加胞質Cyt C蛋白的錶達和P53在線粒體的轉位併誘導ACC-M細胞凋亡。用PFT預處理後,icotinib誘導ACC-M細胞的凋亡明顯下降,線粒體蛋白P53的錶達降低,胞質內Cyt C錶達減少, Caspase-3凋亡相關蛋白活力下降。結論 icotinib可能通過誘導P53轉位到線粒體進而促進ACC-M細胞凋亡。
목적이용연선선양낭성암세포계ACC-M세포위모형,연구불동농도애극체니( icotinib)대연선선양낭성암세포계ACC-M세포조망적영향이급선립체재 icotinib 유도ACC-M세포조망중적작용。방법 icotinib 화 P53억제제( PFT)분별처리ACC-M세포,응용새서람비색법검측세포활성,이용 Western blot 법검측 P53화포질내세포색소 C ( Cyt C)단백적표체변화,용Caspase-3조망상관단백활력검측ACC-M세포적조망정황。결과 icotinib가억제ACC-M세포적활성,증가포질Cyt C단백적표체화P53재선립체적전위병유도ACC-M세포조망。용PFT예처리후,icotinib유도ACC-M세포적조망명현하강,선립체단백P53적표체강저,포질내Cyt C표체감소, Caspase-3조망상관단백활력하강。결론 icotinib가능통과유도P53전위도선립체진이촉진ACC-M세포조망。
Objective To investigate the role of mitochondrion in the induction of the apoptosis in human salivary adenoid cystic carcinoma cells through icotinib and to observe the effect of different concentrations of icotinib on the apoptosis. Methods The ACC-M cells were exposed to icotinib and ( or) the P53 inhibitor PFT. The cell viability of ACC-M was measured by MTT assay. Expression of P53 and Cyt C was determined by Western blot analysis. The apoptosis of ACC-M cells was measured by Caspase-3 apoptosis related protein activity. Results icotinib inhib-ited the viability in ACC-M. icotinib significantly increased the protein levels of P53 in mitochondrion and Cyt C in cytoplasm and induced apoptosis in ACC-M. However, pretreatment with P53 inhibitor( PFT) , the inhibitory effect of icotinib on ACC-M cells was significantly reversed. The level of the Caspase-3 apoptosis related protein activity and the expression of P53 in mitochondrion and Cyt C in cytoplasm were also decreased significantly. Conclusionicotinib may induce apoptosis of ACC-M through the P53 mitochondrial translocation.