[1]刘志峰 陈永汉 姜 浩.AMOTL2与FKBP51表达水平与胶质母细胞瘤病人预后的关系[J].中国临床神经外科杂志,2021,26(10):780-783.[doi:10.13798/j.issn.1009-153X.2021.10.011]
 LIU Zhi-feng,CHEN Yong-han,JIANG Hao.Relationship between AMOTL2 and FKBP51 expression and prognoses of glioblastoma patients[J].,2021,26(10):780-783.[doi:10.13798/j.issn.1009-153X.2021.10.011]
点击复制

AMOTL2与FKBP51表达水平与胶质母细胞瘤病人预后的关系()
分享到:

《中国临床神经外科杂志》[ISSN:1009-153X/CN:42-1603/TN]

卷:
26
期数:
2021年10期
页码:
780-783
栏目:
论著
出版日期:
2021-10-25

文章信息/Info

Title:
Relationship between AMOTL2 and FKBP51 expression and prognoses of glioblastoma patients
文章编号:
1009-153X(2021)10-0780-04
作者:
刘志峰 陈永汉 姜 浩
作者单位:061001 河北,沧州市中心医院神经外二科(刘志峰、陈永汉、姜 浩)
Author(s):
LIU Zhi-feng CHEN Yong-han JIANG Hao
Department of Neurosurgery, Cangzhou Central Hospital, Cangzhou 061001, China
关键词:
胶质母细胞瘤类血管动蛋白-2FK506结合蛋白51预后
Keywords:
Glioblastoma Angiomotin like-2 FK506 binding proteins 51 Prognosis
分类号:
A
DOI:
10.13798/j.issn.1009-153X.2021.10.011
文献标志码:
R 739.41; Q 786
摘要:
目的 探讨胶质母细胞瘤(GBM)类血管动蛋白-2(AMOTL2)与FK506结合蛋白51(FKBP51)表达变化及临床意义。方法 收集2016年6月~2019年6月手术切除的GBM标本92例,以取同期颅脑损伤内减压术切除的非肿瘤脑组织48例为对照。采用免疫组化染色法检测AMOTL2、FKBP51表达。GBM病人术后随访2年,记录无进展生存期和总生存期。结果 GBM组织AMOTL2低表达率、FKBP51高表达率均明显高于对照组(P<0.05)。GBM组织AMOTL2表达水平与P53、EGFR呈明显负相关(P<0.05),FKBP51表达水平与P53、EGFR呈明显正相关(P<0.05)。Cox比例回归风险模型分析显示,AMOTL2低表达、FKBP51高表达是GBM生存预后不良的独立危险因素(P<0.05)。生存曲线分析显示,AMOTL2高表达组病人无进展生存期、总生存期较低表达组均明显延长(P<0.05),FKBP51高表达组无进展生存期、总生存期较低表达组均明显缩短(P<0.05)。结论 GBM组织AMOTL2呈低表达,而FKBP51呈高表达,二者均与P53、EGFR表达相关,与病人预后密切相关。
Abstract:
Objective To explore the expression changes of angiomotin-2 (AMOTL2) and FK506 binding protein 51 (FKBP51) in glioblastoma (GBM) tissues and their clinical significance. Methods The expression levels of AMOTL2 and FKBP51 were detected in GBM tissues obtained from 92 GBM patients who underwent microsurgery from June 2016 to June 2019 and in non-tumor cerebral tissues obtained from 48 patients (control) with traumatic brain injury who underwent decompression during the same period by immunohistochemical staining. The patients with GBM were followed up for 2 years, and the progression-free survival (PFS) and overall survival (OS) were recorded. Results The low expression rate of AMOTL2 and the high expression rate of FKBP51 in GBM tissues were significantly higher than those in the control group (P<0.05). The expression level of AMOTL2 in GBM tissues was significantly negatively correlated with P53 and EGFR (P<0.05), and the expression level of FKBP51 was significantly positively correlated with P53 and EGFR (P<0.05). Cox proportional regression risk model analysis showed that low expression of AMOTL2 and high expression of FKBP51 were independent risk factors for poor survival prognoses of GBM patients (P<0.05). Survival curve analysis showed that the PFS and OS of patients in the AMOTL2 high-expression group were significantly prolonged compared to the low-expression group (P<0.05). The PFS and OS of patients in the FKBP51 high-expression group were significantly shortened compared to the low-expression group (P<0.05). Conclusions The expression of AMOTL2 in GBM tissue is low, while the expression of FKBP51 is high. Both of them are related to the expression of P53 and EGFR in GBM tissues, and are closely related to the GBM patient’s prognosis.

参考文献/References:

[1] 彭 倩,韩 刚,张志辰,等. 胶质母细胞瘤差异表达基因的生物信息学分析[J]. 现代肿瘤医学,2020,28:58-63.
[2] Meng L, Shen Y, Jiao Y, et al. Angiomotin family members: oncogenes or tumor suppressors [J]. Int J Biol Sci, 2017, 13(6): 772-781.
[3] Takaoka M, Ito S, Miki Y, et al. FKBP51 regulates cellmotility and invasion via RhoA signaling [J]. Cancer Sci, 2017, 108(3): 380-389.
[4] 陈 杰. 病理诊断免疫组化手册[M]. 北京:中国协和医科大学出版社,2014. 77.
[5] Kim M, Park SJ, Lee C, et al. Role of Angiomotin-like 2 mono-ubiquitination on YAP inhibition [J]. EMBO Rep, 2016, 17(1): 64-78.
[6] D’Arrigo P, Russo M, Rea A, et al. A regulatory role for the co-chaperone FKBP51s in PD-L1 expression in glioma [J]. Oncotarget, 2017, 8(40): 68291-68304.
[7] Chen X, Lu Y, Guo G, et al. AMOTL2 knockdown promotes the proliferation, migration and invasion of glioma by regulating β-catenin nuclear localization [J]. Oncol Rep, 2021 ,46(1): 1-11.
[8] Xia Z, Zhang G, Wang C, et al. The role of FKBP51 in the prognosis of ulcerative colitis-associated colorectal cancer[J]. Adv Med Sci, 2021, 66(1): 89-97.
[9] 夏志秀,王昌亮,韩彦槊,等. FKBP51在结直肠癌与正常组织中的表达差异及与临床病理特征的关系[J]. 中国医师杂志,2017,19(3):362-366.
[10] 邢海霞,赵明燕,郭 勇,等. Cat B、p53在脑胶质瘤组织中的表达及临床意义[J]. 现代肿瘤医学,2019,27(8):55-59.
[11] 姜振富,李 梅,韦 鸿. 脑胶质瘤EGFR、KRAS和Ki67蛋白的表达及临床意义[J]. 大连医科大学学报,2017,39(2):127-131.
[12] Russo M, D’Arrigo P, Hausch F, et al. Abstract 2216: Study of PDL-1 regulation and expression in glioblastoma and its role in cancer resistance [J]. Cancer Res, 2016, 76(14 Suppl): 2216-2216.

相似文献/References:

[1]谢宝树 张 林 王 宇 贾 锋 殷玉华.复发性多发胶质母细胞瘤的预后分析[J].中国临床神经外科杂志,2016,(06):333.[doi:10.13798/j.issn.1009-153X.2016.06.005]
 XIE Bao-shu,ZHANG Lin,WANG Yu,et al.Analysis of prognoses in patients with recurrent multiple glioblastomas[J].,2016,(10):333.[doi:10.13798/j.issn.1009-153X.2016.06.005]
[2]宋贵东 综述 高之宪 审校.贝伐单抗治疗复发胶质母细胞瘤的研究进展[J].中国临床神经外科杂志,2015,(10):638.[doi:10.13798/j.issn.1009-153X.2015.10.022]
[3]李继强 杨吉安 邵灵敏 吴庭枫 刘宝辉 陈谦学.稳定低表达BAG3的胶质母细胞瘤U87细胞株的构建及鉴定[J].中国临床神经外科杂志,2015,(06):353.[doi:10.13798/j.issn.1009-153X.2015.06.011]
 LI Ji-qiang,YANG Ji-an,SHAO Ling-min,et al.Construction and identification of U87 glioblastoma cell strain with a stable low expression of BAG3[J].,2015,(10):353.[doi:10.13798/j.issn.1009-153X.2015.06.011]
[4]桂志勇 冯 军 黄俊红 白敬洋.靶向沉默c-fos基因表达对胶质瘤U87MG细胞增殖与侵袭的影响[J].中国临床神经外科杂志,2017,(12):834.[doi:10.13798/j.issn.1009-153X.2017.12.011]
 GUI Zhi-yong,FENG Jun,HUANG Jun-hong,et al.Effects of c-fos targeted silence on proliferation and invasiveness of human glioma cell U87[J].,2017,(10):834.[doi:10.13798/j.issn.1009-153X.2017.12.011]
[5]王娇燕 孟凡华 刘魏然 魏春晓 林丽萍.SWI在胶质母细胞瘤与单发脑转移瘤鉴别中的价值[J].中国临床神经外科杂志,2018,(01):13.[doi:10.13798/j.issn.1009-153X.2018.01.005]
 WANG Jiao-yan,MENG Fan-hua,LIU Wei-ran,et al.Value of susceptibility-weighted imaging in differentiative diagnosis of glioblastomas and solitary brain metastases[J].,2018,(10):13.[doi:10.13798/j.issn.1009-153X.2018.01.005]
[6]张治元 王汉东 樊友武 贾 玥 吴晋蓉.胶质肉瘤15例分析及文献复习[J].中国临床神经外科杂志,2018,(02):69.
 ZHANG Zhi-yuan,WANG Han-dong,FAN You-wu,et al.Diagnosis and treatment of gliosarcoma: a report of 15 cases and literature review[J].,2018,(10):69.
[7]郑锐哲 姜秀峰 陈二涛 孙兆良 冯东福.胶质母细胞瘤卒中术后继发硬膜下水瘤1例[J].中国临床神经外科杂志,2019,(02):128.[doi:10.13798/j.issn.1009-153X.2019.02.022]
[8]胡 玥,薛小燕,李子超,等.阿苯达唑抑制胶质瘤裸鼠模型肿瘤生长[J].中国临床神经外科杂志,2019,(06):348.[doi:10.13798/j.issn.1009-153X.2019.06.010]
 HU Yue,XUE Xiao-yan,LI Zi-chao,et al.Albendazole inhibits tumor growth in nude mice model of glioma[J].,2019,(10):348.[doi:10.13798/j.issn.1009-153X.2019.06.010]
[9]殷安安 陆 南 贺亚龙 章 翔 刘玉河.TRIM38基因非CpG岛DNA甲基化与胶质母细胞瘤临床预后的关系[J].中国临床神经外科杂志,2020,(02):76.[doi:10.13798/j.issn.1009-153X.2020.02.005]
 YIN An-an,LU Nan,HE Ya-long,et al.Impacts of TRIM38 non-CpG island DNA methylation alterations on clinical prognosis in patients with glioblastomas[J].,2020,(10):76.[doi:10.13798/j.issn.1009-153X.2020.02.005]
[10]吴 蛟 易 勇 赵卓琳 周良学 周世军.贝伐珠单抗联合化疗治疗胶质母细胞瘤的meta分析[J].中国临床神经外科杂志,2020,(02):82.[doi:10.13798/j.issn.1009-153X.2020.02.007]
 WU Jiao,YI Yong,ZHAO Zhuo-lin,et al.Efficacy and safety of bevacizumab combined with chemotherapy for glioblastoma: a meta-analysis[J].,2020,(10):82.[doi:10.13798/j.issn.1009-153X.2020.02.007]

更新日期/Last Update: 1900-01-01