Pacilitaxel induces human nasopharyngeal carcinoma cell line CNE2 apoptosis and growth inhibition by suppressing PI3K/AKT/p53 signaling pathway
-
摘要: 目的: 探讨紫杉醇(PTX)对人鼻咽癌细胞株CNE2的作用及机制。方法: 取对数生长期的CNE2细胞分别用不同浓度(0、5、10、20 mol/L)的PTX处理。细胞培养72 h后,利用MTT检测细胞增殖;流式检测细胞凋亡和膜电位;免疫印迹法检测PI3K,p-AKT,AKT,p53,p21,Caspase3,Cleavage-Caspase3,PARP,Cleavage-PARP,CytC,AIF,Bcl-2和Bax表达。结果: PTX呈浓度依赖性诱导CNE2细胞增殖抑制和凋亡,增加Caspase3、PARP、CytC、AIF和Bax表达,下调PI3K、p-AKT、p53、p21、Cleavage-PARP、Cleavage-Caspase3和Bcl-2的表达和细胞膜电位,但对AKT表达无明显影响。结论: PTX可通过抑制PI3K/AKT/p53信号通路而诱导CNE2细胞增殖抑制和凋亡。Abstract: Objective To investigate the effect and mechanisms of the PTX on the human nasopharyngeal carcinoma cell line CNE2.Method: Cells from CNE2 were cultured in vitro and the cells at logarithmic growth phase were processed with different concentration of PTX(0,5, 10, 20) mol/L for 72h. MTT was used to evaluate the proliferation and flow cytometric analysis was utilized to detect membrane potential and apoptosis of CNE2 cells. The expression of PI3K, p-AKT,AKT, p53,p21, Caspase3, Cleavage-Caspase3, PARP, Cleavage-PARP, AIF, CytC, Bcl-2 and Bax in CNE2 cells were examined by Western Blot.Result: The results showed that PTX could increase the apoptosis and the expression of Caspase3, PARP, CytC, AIF and Bax and reduce the proliferation, membrane potential and the expression of PI3K, p-AKT, p53, p21, Cleavage-PARP, Cleavage-Caspase3 and Bcl-2 in CNE2 cell in a concentration-dependent manner. However, PTX had no effect on the expression of AKT.Conclusion: PTX can promote apoptosis and growth inhibition of human nasopharyngeal cancer cell line CNE2 and the mechanism involves suppressing PI3K/AKT/p53 signaling pathway.
-
Key words:
- nasopharyngeal neoplasms /
- pacilitaxel /
- proliferation /
- apoptosis
-
-
[1] KAMRAN S C,RIAZ N,LEE N.Nasopharyngeal carcinoma[J].Surg Oncol Clin N Am,2015,24:547-561.
[2] PETERSSON F.Nasopharyngeal carcinoma:a review[J].Semin Diagn Pathol,2015,32:54-73.
[3] 刘超,李果,刘勇,等.miRNA-324-3p及其靶基因WNT2B在鼻咽癌组织中的表达及临床意义[J].临床耳鼻咽喉头颈外科杂志,2014,28(21):1676-1684.
[4] ONISHI Y,ESHITA Y,JI R C,et al.Anticancer efficacy of a supramolecular complex of a 2-diethylaminoethyl-dextran-MMA graft copolymer and paclitaxel used as an artificial enzyme[J].Beilstein J Nanotechnol,2014,5:2293-2307.
[5] LI Y,ZHANG G,PFEIFER B A.Current and emerging options for taxol production[J].Adv Biochem Eng Biotechnol,2015,148:405-425.
[6] GOEL A,AGGARWAL B B.Curcumin,the golden spice from Indian saffron,is a chemosensitizer and radiosensitizer for tumors and chemoprotector and radioprotector for normal organs[J].Nutr Cancer,2010,62:919-930.
[7] 孔建强,王伟,朱平,等.紫杉醇生物合成的研究进展[J].药学学报,2007,42(4):358-365.
[8] GANDHI S,FLETCHER G G,EISEN A,et al.Adjuvant chemotherapy for early female breast cancer:a systematic review of theevidence for the 2014 Cancer Care Ontario systemic therapy guideline[J].Curr Oncol,2015,22(Suppl 1):S82-94.
[9] SHAN X,LI Y,MENG X,et al.Curcumin and(-)-epigallocatechin-3-gallate attenuate acrylamideinduced proliferation in HepG2 cells[J].Food Chem Toxicol,2014,66:194-202.
[10] JUHASZOVA M,ZOROV D B,KIM S H,et al.Glycogen synthase kinase-3beta mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore[J].J Clin Invest,2004,113:1535-1549.
[11] WEISS J N,KORGE P,HONDA H M,et al.Role of the mitochondrial permeability transition in myocardial disease[J].Circ Res,2003,93:292-301.
[12] JIE B,ZHANG X,WU X,et al.Neuregulin-1suppresses cardiomyocyte apoptosis by activating PI3K/Akt and inhibitingmitochondrial permeability transition pore[J].Mol Cell Biochem,2012,370:35-43.
[13] YING L,ZHU Z,XU Z,et al.Cancer Associated Fibroblast-Derived Hepatocyte Growth Factor Inhibits the Paclitaxel-Induced Apoptosis ofLung Cancer A549 Cells by Up-Regulating the PI3K/Akt and GRP78 Signaling on a Microfluidic Platform[J].PLoS One,2015,10:e0129593.
-
计量
- 文章访问数: 74
- PDF下载数: 41
- 施引文献: 0
下载: