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TAE684联合克唑替尼对H2228耐药细胞的影响

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摘要 背景:ALK抑制剂克唑替尼及TAE684可以通过阻断smad信号通路来实现H2228细胞的抑制生长和促进凋亡。目的:探究TAE684+克唑替尼对耐药细胞的影响(基于H2228耐药后)。方法:对H2228细胞进行处理(根据不同的实验需要),分别选取30,90,270,810nmol/L的克唑替尼对肺腺癌H2228细胞株耐药性(采取逐步递增法)进行检测。结果与结论:ALK抑制剂克唑替尼及TAE684对EML4-ALK融合基因阳性人肺癌细胞株H2228细胞的凋亡具有促进作用,而且对时间和剂量具有较高的依赖性;凋亡的H2228细胞株的活化水平明显下降,且处于关键蛋白下游的活化水平下降程度更为凸显;EML4-ALK融合基因阳性的表达式未受影响,但是其活化形式明显的受到抑制。实验证明:TAE684联合ALK抑制剂克唑替尼对耐克唑替尼EML4-ALK融合基因阳性人肺癌细胞株H2228细胞的凋亡具有促进作用。
作者 高海祥
出处 《中国组织工程研究》 CAS 北大核心 2016年第B05期107-108,共2页 Chinese Journal of Tissue Engineering Research
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  • 1周韶璋,宋向群,曾爱屏,王惠临,宁瑞玲,于起涛.Bim在克唑替尼诱导EML4-ALK融合基因阳性肺腺癌细胞株H2228凋亡中的作用机制[J].临床肿瘤学杂志,2014,19(8):690-695. 被引量:4
  • 2潘星辰,周韶璋,戴辉,韦江,彭海燕,宋向群.低氧诱导因子-1α mRNA在克唑替尼诱导H2228细胞凋亡中的作用[J].广东医学,2014,35(13):1980-1983. 被引量:2
  • 3张一方.EML4-ALK融合型非小细胞肺癌特性的生物信息学分析及下游STAT3基因的功能验证[D].南方医科大学,2012,27(11):278-279.
  • 4Molina JR, Yang P, Cassivi SD, et al. Non-small cell lung cancer: epidemiology, risk factors, treatment, and survivorship. Mayo Clin Proc: 2008;83(5):584-594.
  • 5Shaw AT, Yeap BY, Solomon B J, et al. Effect of crizotinib on overall survival in patients with advanced non-small-cell lung cancer harbouring ALK gene rearrangement: a retrospective analysis. Lancet Oncol 2011;1201) : 1004-1012.
  • 6Sasaki T, Koivunen J, Ogino A, et al. A novel ALK secondary mutation and EGFR signaling cause resistance to ALK kinase inhibitors. Cancer Res. 2011; 71(18): 6051-6060.
  • 7NCCN Guidelines Non-SmaU cell Lung Cancer 2015 Version 3. NSCL-18.
  • 8lacono D, Chiari R, Metro G, et al. Future options for ALK-positive non-small cell lung cancer, Lung Cancer 2015;87(3):211-219.

二级参考文献34

  • 1Okamoto I, Nakagawa K. Echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase-targeted therapy for advanced non-small cell lung cancer: molecular and clinical as- pects[J]. Cancer Sci, 2012, 103(8) :1391-1396.
  • 2Costa DB, Halmos B, Kumar A, et al. BIM mediates EGFR tyrosine kinase inhibitor-induced apoptosis in lung cancers with ancogenic EGFR mutations[ J]. PLoS Med, 2007, 4 (10) :1669 -1679.
  • 3Ola MS, Nawaz M, Ahsan H. Role of Bcl-2 family proteins and caspases in the regulation of apoptosis [ J ]. Mol Cell Biochem, 2011,351 (1-2) :41-58.
  • 4Kaliberov SA, Buchsbaum D J, Gillespie GY, et al. Adenovirus- mediated transfer of BAX driven by the vascular endothelial growth factor promoter induces apoptosis in lung cancer cells [ J ]. Mol Ther,2002,6(8) : 190-198.
  • 5Gilley J, Coffer P J, Ham J. FOXO transcription factors directly ac- tivate him gene expression and promote apoptosis in sympathetic neurons[J]. J Cell Biol, 2003,162(4) :613-622.
  • 6Essall A, Fernandez MS, Hassen YA, et al. Direct transcriptio- nal regulation of Bim by FOXO3a mediates ST15 71-induced ap- optosis in Ber-Abl-expressing cells [ J ]. Oncogene, 2005, 24(14) : 2317-2329.
  • 7Biswas SC, Liu DX, Greene LA, et al. Bim is a direct target of a neuronal E2F-dependent apoptotic pathway [ J ]. J Neurosci, 2005, 25 (37) : 8349-8358.
  • 8Yano T, Kosei I, Hiroxhi F, et al. The RUNX3 tumor suppressor upregulates Bim in gastric epithelial ceils undergoing transforming growth factorβ-induced apoptosis [ J ]. Mol Cell Biol, 2006, 26 (12) :4474-4488.
  • 9Putcha GV, Le S, Frank S, et al. JNK-mediated Bim phospho- rylation potentiates Bax-dependent apoptosis[ J]. Neuron, 2003, 38(6) :899-914.
  • 10Shaw AT, Kim DW, Nakagawa K, et al. Crizotinib versus chemo- therapy in advanced ALK-positive lung cancer [ J ]. N Engl J Med,2013, 368(25): 2385-2394.

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