肿瘤药学
腫瘤藥學
종류약학
Anti-Tumor Pharmacy
2015年
5期
353-356
,共4页
PIAsxα%鼻咽癌%细胞周期蛋白 D%周期蛋白依赖性激酶
PIAsxα%鼻嚥癌%細胞週期蛋白 D%週期蛋白依賴性激酶
PIAsxα%비인암%세포주기단백 D%주기단백의뢰성격매
PIAsxα%Nasopharyngealcarcinoma%CyclinD%CDK
目的:探讨PIAsxα对鼻咽癌细胞凋亡和成瘤能力的影响及可能机制。方法采用实时定量PCR,流式细胞术以及裸鼠成瘤实验分析PIAsxα在鼻咽癌组织中的表达情况,PIAsxα对鼻咽癌细胞系CNE1凋亡和cyclin D、CDK表达及其成瘤能力的影响。结果鼻咽癌组织中PIAsxα mRNA的表达水平显著低于邻近正常鼻咽组织。过表达PIAsxα的CNE1细胞凋亡率及G2/M期细胞比例均明显增高,cyclin D1、cyclin D3、CDK4、CDK6和CDK8的mRNA表达均显著降低且在裸鼠体内的成瘤能力亦受到抑制。结论PIAsxα的表达下调可能通过增加cyclin D和CDK的表达,抑制鼻咽癌细胞的凋亡,促进鼻咽癌的发生和发展。
目的:探討PIAsxα對鼻嚥癌細胞凋亡和成瘤能力的影響及可能機製。方法採用實時定量PCR,流式細胞術以及裸鼠成瘤實驗分析PIAsxα在鼻嚥癌組織中的錶達情況,PIAsxα對鼻嚥癌細胞繫CNE1凋亡和cyclin D、CDK錶達及其成瘤能力的影響。結果鼻嚥癌組織中PIAsxα mRNA的錶達水平顯著低于鄰近正常鼻嚥組織。過錶達PIAsxα的CNE1細胞凋亡率及G2/M期細胞比例均明顯增高,cyclin D1、cyclin D3、CDK4、CDK6和CDK8的mRNA錶達均顯著降低且在裸鼠體內的成瘤能力亦受到抑製。結論PIAsxα的錶達下調可能通過增加cyclin D和CDK的錶達,抑製鼻嚥癌細胞的凋亡,促進鼻嚥癌的髮生和髮展。
목적:탐토PIAsxα대비인암세포조망화성류능력적영향급가능궤제。방법채용실시정량PCR,류식세포술이급라서성류실험분석PIAsxα재비인암조직중적표체정황,PIAsxα대비인암세포계CNE1조망화cyclin D、CDK표체급기성류능력적영향。결과비인암조직중PIAsxα mRNA적표체수평현저저우린근정상비인조직。과표체PIAsxα적CNE1세포조망솔급G2/M기세포비례균명현증고,cyclin D1、cyclin D3、CDK4、CDK6화CDK8적mRNA표체균현저강저차재라서체내적성류능력역수도억제。결론PIAsxα적표체하조가능통과증가cyclin D화CDK적표체,억제비인암세포적조망,촉진비인암적발생화발전。
Objective To investigate the effect and possible mechanism of PIAsxαon the apoptosis and tumorigenesis of nasopharyngeal carcinoma cells. Method Real-time quantitative PCR, flow cytometry and nude mice tumor forming experiment were applied to analyze the expression of PIAsxαin nasopharyngeal carcinoma (NPC), as well as the impacts of PIAsxαon CNE1 apoptosis, expressions of cyclin D and CDK, and tumorigenicity. Results The mRNA expression levels of PIAsxαin NPC were significantly lower than those in adjacent normal tissue of nasopharyngeal carcinoma. The apoptotic rate and the percentage of G2/M phase cells of PIAsxαoverexpressed CNE1 cells were significantly increased. The mRNA expressions of cyclin D1, cyclin D3, CDK4, CDK6 and CDK8 were significantly decreased. The tumori-genicity in nude mice of PIAsxαoverexpressed CNE1 cells were also significantly inhibited. Conclusion Down-regulation of PIAsxαcould enhance the expressions of cyclin D and CDK, inhibit the apoptosis of nasopharyngeal carcinoma cells and promote the development of na-sopharyngeal carcinoma.