解放军医学杂志2012，Vol.37Issue(6)：569-572,4.
分化抑制因子1对鼻咽癌细胞增殖的影响及其途径
Effect and pathway of Id1 on the cell growth of nasopharyngeal carcinoma
李春燕 1江山 2岳渝娟 2陈晓品2
作者信息
- 1. 400016重庆 重庆医科大学附属第一医院内分泌乳腺外科
- 2. 400016重庆 重庆医科大学附属第一医院肿瘤科
- 折叠
摘要
Abstract
Objective To investigate the effects of Idl on proliferation and apoptosis of nasopharyngeal carcinoma (NPC) cells in vitro and its mechanism. Methods Human nasopharyngeal carcinoma cell NP69 and CNE1 were cultured in vitro. Small interfering RNA and expression vector of Idl were transfected into NP69 and CNE1 cells respectively. NP69 cells transfected with Idl siRNA or control plasmid Scramble for 72h (named NP69si-Idl and NP69-NC respectively), and CNE1 cells transfected with pcDNA3.1- Idl and control pcDNA3.1 for 48h (named CNE1-Id1 and CNEl-Vector respectively) were collected. The effect of siRNA or pcDNA3.1-Idl on the expression level of Idl was evaluated by reverse transcriptase-PCR and Western blotting. MTT assay was performed to compare the effects of DDP on proliferation of both CNEl-Idl and CNEl-Vector and both NP69si-Idl and NP69-NC. CalcuSyn software was used to calculate the IC50 values of cells to cisplatin (DDP). After the lμg/ml DDP and nasopharyngeal carcinoma cells were coincubated for 24 hours, the expressions of cell apoptotic protein caspase-3, Bax, Bad, and the Thr308 and Ser473 phosphorylation of protein kinase B (Akt) were analyzed by Western blotting. Results Obviously lower Idl mRNA and protein levels were detected in NP69si-Idl cells as compared with NP69-NC cells and obviously higher Id l mRNA and protein levels in CNEl-Idl cells than in CNEl-Vector were found. The IC50 value of the NP69si-Idl cells for DDP (0.207 ± 0.008|xg/ ml) was significantly lower than the NP69-NC cells (0.405 ± 0.009μg/ml, P<0.05), and the IC50 value of CNEl-dl cells for DDP (0.671 ± 0.012M-g/ml) was significantly higher than that of CNEl-Vector (0.445 ± 0.008/ml, P<0.05). Western blotting results indicated that the fault zone of caspase-3 increased, and Akt phosphorylation at Thr308 and Ser473 decreased in NP69si-Idl than in NP69-NC, while the fault zone decreased, and Akt phosphorylation at Thr308 and Ser473 increased more significantly in CNEl-Idl than in CNEl-Vector. Conclusion Idl can promote the proliferation of nasopharyngeal carcinoma cells and resist the apoptosis induced by DDP, and the mechanism may be related to the up-regulation of p-Akt.关键词
分化抑制因子1/鼻咽肿瘤/RNA干扰/AKT途径Key words
inhibitor of differentiation l/ naso-pharyngeal neoplasms/ RNA interference/ AKT pathway分类
医药卫生引用本文复制引用
李春燕,江山,岳渝娟,陈晓品..分化抑制因子1对鼻咽癌细胞增殖的影响及其途径[J].解放军医学杂志,2012,37(6):569-572,4.
