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泛素连接酶FBW7在胶质瘤的表达和作用分析 被引量:1

The expressions of ubiquitin ligase FBW7 and its effect on the malignancies in glioma
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摘要 目的研究泛素连接酶FBW7在胶质瘤的表达情况,及其对胶质瘤细胞恶性生物行为的影响。方法应用免疫组织化学染色检测并定量分析FBW7在30例高级别、低级别胶质瘤的蛋白表达情况与表达差异。构建FBW7过表达慢病毒,并转染胶质瘤细胞株U251和U373,MTT法、细胞侵袭实验、划痕实验观察细胞增殖、侵袭和迁移。结果 FBW7在胶质瘤标本中的染色分数低于瘤旁脑组织,在Ⅳ级胶质瘤中的染色分数低于Ⅱ级(P <0.01);与肿瘤增殖标志Ki-67染色水平呈负相关(r=-0.4677)。过表达FBW7的U251和U373细胞增殖、侵袭和迁移能力显著抑制(P <0.01)。结论 FBW7表达随胶质瘤病理级别增加而下调,与增殖程度呈负相关,增加FBW7表达水平可抑制细胞恶性生物行为。 Objective To study the expressions of ubiquitin ligase FBW7 and its effect on the malignancies in glioma. Methods Immunohistological staining was used to detect and quantitatively analyze the expression and expression difference of FBW7 in 30 samples of high grade and low grade gliomas. A FBW7 overexpression lentivirus was generated and transfected into U251 and U373 cell lines for subsequent MTT, transwell and wound healing assay. Results The FBW7 staining scores of glioma tissues were obviously deceased compared with adjacent normal tissues, with a much lower score in Grade Ⅳ than in Grade Ⅱ(P < 0.01). The expressions of FBW7 were negatively correlated with the Ki-67 staining scores( r =-0.4677). The proliferation, invasion and migration were significantly inhibited in FBW7 overexpression of U251 and U373 cells(P < 0.01). Conclusions The expression of FBW7 is down-regulated with the increase of glioma pathological grade, which is negatively correlated with the degree of proliferation.Increasing the expression level of FBW7 can inhibit the malignant behavior of glioma cells.
作者 林靖 宋朝理 张炜 程宏伟 郑小强 高瑞庭 Lin Jing;Song Chaoli;Zhang Wei;Cheng Hongwei;Zheng Xiaoqiang;Gao Ruiting(Department of Neurosurgery,General Hospital of Western Air Force,Chengdu,Sichuan 610021,China)
出处 《中国微侵袭神经外科杂志》 CAS 2018年第11期512-515,共4页 Chinese Journal of Minimally Invasive Neurosurgery
基金 四川省医学科研基金(编号:S15005)
关键词 神经胶质瘤 泛素蛋白连接酶类 检测 免疫组织化学 glioma ubiquitin-protein ligases suppression detection,immunohistochemistry
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  • 1Wolfgang CL, Herman JM, Laheru DA, et al. Recent progress in pancreatic cancer. CA Cancer J Clin 2013; 63:318-348.
  • 2Vincent A, Herman J, Schulick R, Hruban RH, Goggins M. Pancreatic cancer. Lancet 2011; 378:607-620.
  • 3Poruk KE, Firpo MA, Adler DG, Mulvihill SJ. Screening for pancreatic cancer: why, how, and who? Ann Surg 2013; 257:17-26.
  • 4Winter JM, Cameron JL, Campbell KA, et al. 1423 pancreati- coduodenectomies for pancreatic cancer: a single-institution experience. J Gastrointest Surg 2006; 10:1199-1210.
  • 5Iacobuzio-Donahue CA, Velculescu VE, Wolfgang CL, Hruban RH. Genetic basis of pancreas cancer development and progression: insights from whole-exome and whole-ge- nome sequencing. CIin Cancer Res 2012; 18:4257-4265.
  • 6Iacobuzio-Donahue CA. Genetic evolution of pancreatic cancer: lessons learnt from the pancreatic cancer genome se- quencing project. Gut 2012; 61:1085-1094.
  • 7Pdrez-Mancera PA, Guerra C, Barbacid M, Tuveson DA. What we have learned about pancreatic cancer from mouse models. Gastroenterology 2012; 142:1079-1092.
  • 8Welcker M, Clurman BE. FBW7 ubiquitin ligase: a tumour suppressor at the crossroads of cell division, growth and dif- ferentiation. Nat Rev Cancer 2008; 8:83-93.
  • 9Knuutila S, Aalto Y, Autio K, et al. DNA copy number losses in human neoplasms. Am JPathol 1999; 155:683-694.
  • 10Inuzuka H, Shaik S, Onoyama I, et al. SCF (FBWT) regulates cellular apoptosis by targeting MCL1 for ubiquitylation and destruction. Nature 2011; 471:104-109.

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