期刊文献+

沉默BCAT1对肺癌细胞增殖、迁移及侵袭能力的影响 被引量:4

Effect of BCAT1 Knockdown on the Proliferation, Migration and Invasion of Lung Cancer Cells
原文传递
导出
摘要 目的:研究BCAT1在肺癌细胞A549的增殖、迁移及侵袭能力中的作用。方法:通过小干扰RNA(si RNA)沉默A549细胞中BCAT1的表达,细胞分为对照组(Con)、BCAT1基因沉默组(si RNA-BCAT1)和si RNA阴性对照组(si RNA-NC)。利用Western blot检测si RNA对BCAT1的沉默效果;划痕愈合实验检测沉默BCAT1后A549细胞迁移能力的改变;Transwell小室侵袭实验检测沉默BCAT1后A549细胞侵袭能力的变化;MTT实验检测沉默BCAT1对A549细胞增殖能力的影响。结果:与Con组相比,si RNA-BCAT1组的BCAT1蛋白表达明显降低(P<0.05),细胞划痕愈合率明显降低(P<0.05),能够穿膜的细胞数明显减少(P<0.05),而Con组和si RNA-BCAT1组细胞的增殖能力比较差异无明显统计学意义(P>0.05)。结论:沉默BCAT1抑制A549细胞的迁移和侵袭能力,而对其增殖能力无影响。 Objective: To investigate the effect of BCAT1 on the proliferation, migration and invasion of lung cancer A549 cells. Methods: BCAT1 was knocked down by siRNA and A549 cells were divided into three groups: control group, siRNA-BCAT1 group and siRNA-NC group. Western blot was performed to detect the expression ofBCAT1. Cell migration was tested by wound healing assay and cell invasion was evaluated by Transwell assay. MTT assay was performed to investigate the effect of BCAT1 knockdown on the cell proliferation. Results: Compared with those of the control group and siRNA-NC group, the protein expression of BCAT1 in A549 cells of siRNA-BCAT1 group was significantly decreased (P〈0.05), the rate of wound healing was decreased (P〈0.05) and the cell invasion was suppressed(P〈0.05). However, no significnat difference was found in the MTT assay results between three groups(P〉0.05). Conclusion: Knockdown of the BCAT1 expression in A549 cells resulted in significant decrease of cell migration and invasion but had no impact on the proliferation of lung cancer A549 cells.
出处 《现代生物医学进展》 CAS 2017年第34期6644-6647,6643,共5页 Progress in Modern Biomedicine
基金 陕西省自然科学基金面上项目(2016JM8009)
关键词 肺癌 BCATl 迁移 侵袭 增殖 Lung cancer BCAT1 Migration Invasion Proliferation
  • 相关文献

参考文献2

二级参考文献24

  • 1Chen YJ, Lin SC, Kao T, et al. Genome-wide profiling of oral squamous cell carcinoma[J]. J Pathol, 2004, 204(3): 326-32.
  • 2Noutomi Y, Oga A, Uchida K, et al. Comparative genomic hybridization reveals genetic progression of oral squamous cell carcinoma from dysplasia via two different tumourigenic pathways[J]. J Pathol, 2006; 210(1): 67-74.
  • 3Jin C, Jin Y, Wennerberg J, et al. Cytogenetic abnormalities in 106 oral squamous cell carcinomas [J]. Cancer Genet Cytogenet, 2006; 164(1): 44-53.
  • 4Garnis C, Chari R, Buys TP, et al. Genomic imbalances in precancerous tissues signal oral cancer risk[J]. Mol Cancer, 2009, 23; 8:50.
  • 5Durkin ME, Yuan BZ, Zhou X, et al. DLC-1 :a Rho GTPase-activating protein and tumour suppressor [J]. J Cell Mol Med, 2007,11 (5):1185-207.
  • 6Hewitt C, Wilson P, McGlinn E, et al. DLC1 is unlikely to be a primary target for deletions on chromosome arm 8p22 in head and neck squamous cell carcinoma[J]. Cancer Lett, 2004, 209(2): 207-13.
  • 7Coupade C, Gillet R, Bennoun M, et al. Annexinl expression and phosphorylation are upregulated during liver regeneration and transformation in antithrombin Ⅲ SV40T large antigen transgenic mice[J]. Hepatology.2000; 31(2):372.
  • 8Pencil SD, Toth M. Elevated levels of annexinl protein in vitro and in vivo in rat and human mammary adenocarcinoma [J]. Clin Exp Metastasis.1998; 16(2):113.
  • 9Cloud P. Paweletz, David K. Omstein, et al. Loss of annexin lcorrelates with early onset of tumorigenesis in esophageal and prostate carcinoma[J]. Cancer Res, 2000; 60:6293-6297.
  • 10Hermsen MA, Xie Y, Rooimans MA, et al. Cytogenetic characteristics of oral squamous cell carcinomas in Fanconi anemia[J]. Faro Cancer, 2001, 1(1): 39-43.

共引文献6

同被引文献33

引证文献4

二级引证文献5

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部