实用肿瘤学杂志
實用腫瘤學雜誌
실용종류학잡지
JOURNAL OF PRACTICAL ONCOLOGY
2015年
1期
22-28
,共7页
自噬%他莫昔芬%LC3%p38%c-Jun
自噬%他莫昔芬%LC3%p38%c-Jun
자서%타막석분%LC3%p38%c-Jun
Autophagy%Tamoxifen%LC3%p38%c-Jun
目的：探讨自噬在乳腺癌细胞中对他莫昔芬耐药的影响。方法免疫荧光法计数MCF－7及MCF－7／TAMR中含有自噬体的细胞比例及平均每个细胞中自噬体的个数；蛋白印迹法检测MCF－7和MCF－7／TAMR中p38、c－Jun和LC3表达的差异；逐步法检测当LC3的表达改变时，产生耐药细胞株时间的差异。结果与MCF－7比较，MCF－7／TAMR中含有自噬体的细胞比例及平均每个细胞中自噬体的个数均明显增多；MCF－7／TAMR中LC3蛋白的表达水平明显增高；在诱导TAM耐药过程中LC3的表达水平与耐药细胞株的产生时间呈负相关。在MCF－7／TAMR中磷酸化的p38和c－Jun表达明显增加。结论自噬促进乳腺癌细胞对他莫昔芬耐药，通过降低自噬相关蛋白的表达活性能够抑制乳腺癌耐药细胞的产生，这可能成为难治性乳腺癌治疗的新途径。
目的：探討自噬在乳腺癌細胞中對他莫昔芬耐藥的影響。方法免疫熒光法計數MCF－7及MCF－7／TAMR中含有自噬體的細胞比例及平均每箇細胞中自噬體的箇數；蛋白印跡法檢測MCF－7和MCF－7／TAMR中p38、c－Jun和LC3錶達的差異；逐步法檢測噹LC3的錶達改變時，產生耐藥細胞株時間的差異。結果與MCF－7比較，MCF－7／TAMR中含有自噬體的細胞比例及平均每箇細胞中自噬體的箇數均明顯增多；MCF－7／TAMR中LC3蛋白的錶達水平明顯增高；在誘導TAM耐藥過程中LC3的錶達水平與耐藥細胞株的產生時間呈負相關。在MCF－7／TAMR中燐痠化的p38和c－Jun錶達明顯增加。結論自噬促進乳腺癌細胞對他莫昔芬耐藥，通過降低自噬相關蛋白的錶達活性能夠抑製乳腺癌耐藥細胞的產生，這可能成為難治性乳腺癌治療的新途徑。
목적：탐토자서재유선암세포중대타막석분내약적영향。방법면역형광법계수MCF－7급MCF－7／TAMR중함유자서체적세포비례급평균매개세포중자서체적개수；단백인적법검측MCF－7화MCF－7／TAMR중p38、c－Jun화LC3표체적차이；축보법검측당LC3적표체개변시，산생내약세포주시간적차이。결과여MCF－7비교，MCF－7／TAMR중함유자서체적세포비례급평균매개세포중자서체적개수균명현증다；MCF－7／TAMR중LC3단백적표체수평명현증고；재유도TAM내약과정중LC3적표체수평여내약세포주적산생시간정부상관。재MCF－7／TAMR중린산화적p38화c－Jun표체명현증가。결론자서촉진유선암세포대타막석분내약，통과강저자서상관단백적표체활성능구억제유선암내약세포적산생，저가능성위난치성유선암치료적신도경。
Objective To investigate the effects of autophagy on breast cancer cells to tamoxifen resist-ance.Methods Immunofluorescence was used to count the proportion of the cells with autophagy in MCF -7 and MCF-7/TAMR,as well as ,the average of autophagosome in each cells .Western blotting was used to detect the different expressions of p38,c-jun and LC3 in MCF-7 and MCF-7/TAMR.Stepwise selection was used to detect the duration of resistance to different doses of tamoxifen when upregulating or downregulating of LC 3.West-ern blot was facilitated to investigate changes of activity of p 38/c-jun.Rusults Compared with MCF -7,the proportion of the cells with autophagosome in MCF -7/TAMR was markedly increased ,the same as the average of autophagosome in each cells .Compared with MCF-7,LC3,especially LC3IIprotein expressive levels in MCF -7/TAMR was significantly increased .The expressive level of LC3 during the induction process of TAM resistance was negative correlated with resistant cell lines .The expressions of phosphorylated p 38 and c-Jun in MCF-7/TAMR were significantly increased .Conclusion Autophagy promotes breast cancer cells to resistant to tamox-ifen,due to downregulation of the expression of autophagy related proteins which may inhibit the generation of re -sistant breast cancer cells .This may be a viable treatment strategy for refractory breast cancer .
