[1]平建峰　麻来峰　林昌福.miR-126基因启动子甲基化状态与高危低级别胶质瘤同步放化疗后生存结局的关系[J].中国临床神经外科杂志,2021,26(08):603-606.[doi:10.13798/j.issn.1009-153X.2021.08.010]
　PING Jian-feng,MA Lai-feng,LIN Chang-fu..Relationship between promoter methylation status of miR-126 gene and survival outcome of patients with high-risk low-grade glioma after concurrent radiochemotherapy[J].,2021,26(08):603-606.[doi:10.13798/j.issn.1009-153X.2021.08.010]
点击复制

miR-126基因启动子甲基化状态与高危低级别胶质瘤同步放化疗后生存结局的关系()
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08期
页码:
603-606
栏目:
论著
出版日期:
2021-08-25

文章信息/Info

Title:
Relationship between promoter methylation status of miR-126 gene and survival outcome of patients with high-risk low-grade glioma after concurrent radiochemotherapy
文章编号:
1009-153X（2021）08-0603-04
作者:
平建峰　麻来峰　林昌福
Author(s):
PING Jian-feng;  MA Lai-feng;  LIN Chang-fu.
Department of Neurosurgery, The Third People’s Hospital of Henan, Zhengzhou 450006, China
关键词:
低级别胶质瘤; 同步放化疗; miR-126; 启动子甲基化; 生存结局
Keywords:
Low-grade glioma;  Concurrent radiochemotherapy;  miR-126;  Methylation;  Survival outcome
分类号:
R 739.41; Q 786
DOI:
10.13798/j.issn.1009-153X.2021.08.010
文献标志码:
A
摘要:
目的 探讨miR-126基因启动子甲基化状态对高危低级别胶质瘤（LGG）同步放化疗后生存结局的影响。方法 前瞻性收集2015年7月至2016年9月经术后病理证实为高危LGG组织标本共69例，另选取同期颅脑损伤内减压术切除非肿瘤脑组织20例为对照。采用PCR和MSP法检测miR-126水平及其基因启动子甲基化水平。根据实体肿瘤疗效评价标准分为完全缓解（CR）、部分缓解（PR）、疾病稳定（SD）和疾病进展期（PD），其中CR+PR为敏感组，SD+PD为不敏感组。随访截止时间为2021年5月31日，69例胶质瘤随访19~55个月，中位时间27个月；主要终点为无进展生存期（PFS）、总生存期（OS）。结果 胶质瘤组织miR-126水平显著低于非肿瘤脑组织（P<0.001），而胶质瘤组织miR-126基因启动子甲基化率明显高于非肿瘤脑组织（P<0.05）。胶质瘤组织miR-126水平与其基因启动子甲基化率呈明显负相关（r=-0.722，P<0.001）。多因素logistic回归分析显示miR-126基因启动子高甲基化率是高危LGG对同步放化疗不敏感的独立危险因素（P<0.05）。多因素Cox回归分析显示miR-126基因启动子高甲基化率是高危LGG病人PFS、OS明显缩短的独立危险因素（P<0.05）。Kaplan-Meier生存曲线分析显示，miR-126基因启动子甲基化组OS、PFS较非甲基化组明显缩短（P<0.001）。结论 高危LGG组织miR-126水平与启动子甲基化水平呈明显负相关，miR-126基因启动子高甲基化率是高危LGG同步放化疗不良结局的独立危险因素。
Abstract:
Objective To investigate the relationship between the promoter methylation status of miR-126 gene and the survival outcome of patients with high-risk low-grade glioma (LGG) after concurrent radiochemotherapy. Methods PCR and MSP methods were used to detect miR-126 levels and its gene promoter methylation levels in glioma tissues obtained from 69 patients with high-risk LGG who were prospectively recruited from July 2015 to September 2016 and in non-tumor cerebral tissues obtained from 20 patients with tranmatic brain injury who underwent decompression, respectively. According to the evaluation criteria of solid tumors, the efficacy of concurrent radiochemotherapy was divided into complete remission (CR), partial remission (PR), stable disease (SD) and advanced disease (PD), with CR+PR as the sensitive group and SD+PD as the insensitive group. The deadline for follow-up was on May 31, 2021. The follow up of 69 LGG patients ranged from 19 months to 55 months, with a median time of 27 months; the primary endpoints were progression-free survival (PFS) and overall survival (OS). Results The level of miR-126 in glioma tissues was significantly lower than that in non-tumor cerebral tissues (P<0.001), and the methylation rate of miR-126 gene promoter in glioma tissues was significantly higher than that in the non-tumor cerebral tissues (P<0.05). The level of miR-126 in glioma tissues was significantly negatively correlated with its gene promoter methylation rate (r=-0.722, P<0.001). Multivariate logistic regression analysis showed that the high methylation rate of miR-126 gene promoter in glioma tissues was an independent risk factor for the insensitivity of high-risk LGG to concurrent radiochemotherapy (P<0.05). Multivariate Cox regression analysis showed that the high methylation rate of the miR-126 gene promoter in glioma tissues was an independent risk factor for the significant shortening of PFS and OS in high-risk LGG patients (P<0.05). Kaplan-Meier survival curve analysis showed that the OS and PFS of the miR-126 gene promoter methylation group were significantly shorter than those of the non-methylation group (P<0.001). Conclusions The level of miR-126 in high-risk LGG tissues is significantly negatively correlated with its promoter methylation level. The high methylation rate of the miR-126 gene promoter is an independent risk factor for the adverse outcomes of high-risk LGG patients after concurrent radiochemotherapy.

参考文献/References:

[1] Bell EH, Zhang P, Fisher BJ, et al. Association of MGMT promoter methylation status with survival outcomes in patients with high-risk glioma treated with radiotherapy andtemozolomide: an analysis from the NRG Oncology/RTOG 0424 Trial [J]. JAMA Oncol, 2018, 4(10):1405-1409.
[2] 潘　婷，苏春秋，张　璇，等. 常规MRI特征在预测弥漫性低级别胶质瘤1p/19q缺失状态的应用价值[J]. 临床放射学杂志，2020，39（6）：1189-1194.
[3] Balachandran AA, Larcher LM, Chen S, et al. Therapeuti-cally significant microRNAs in primary and metastatic brain malignancies [J]. Cancers (Basel), 2020, 12(9): 2534.
[4] Kim JH, Kim BJ, Jang HJ, et al. Comparison of the RECIST and EORTC PET criteria in the tumor response assessment:a pooled analysis [J]. Cancer Chemother Pharmacol, 2017, 80(4): 729-735.
[5] Buruian? A, Florian ?I, Florian AI, et al. The Roles of miRNA in glioblastoma tumor cell communication: diplo-matic and aggressive negotiations [J]. Int J Mol Sci, 2020, 21(6): 1950.
[6] Yuan M, Da Silva ACAL, Arnold A, et al. MicroRNA (miR) 125b regulates cell growth and invasion in pediatric low grade glioma [J]. Sci Rep, 2018, 8(1): 12506.
[7] Chen SR, Cai WP, Dai XJ, et al. Research on miR-126 in glioma targeted regulation of PTEN/PI3K/Akt and MDM2-p53 pathways [J]. Eur Rev Med Pharmacol Sci, 2019, 23(8): 3461-3470.
[8] Li M, Wang Q, Zhang X, et al. Exosomal miR-126 blocks the development of non-small cell lung cancer through the inhibition of ITGA6 [J]. Cancer Cell Int, 2020, 20(1): 574.
[9] Ouyang J, Song F, Li H, et al. miR-126 targeting GOLPH3 inhibits the epithelial-mesenchymal transition of gastric cancer BGC-823 cells and reduces cell invasion [J]. Eur J Histochem, 2020, 64(4): 3168.
[10] Han L, Liu H, Wu J, et al. MiR-126 suppresses invasion and migration of malignant glioma by targeting mature T cell proliferation 1 (MTCP1) [J]. Med Sci Monit, 2018, 24: 6630-6637.
[11] Xu Y, Xu W, Lu T, et al. miR-126 affects the invasion and migration of glioma cells through GATA4 [J]. Artif Cells Nanomed Biotechnol, 2017, 45(6): 1-7.
[12] Kohanbash G, Carrera DA, Shrivastav S, et al. Isocitrate dehydrogenase mutations suppress STAT1 and CD8+ T cell accumulation in gliomas [J]. J Clin Invest, 2017, 127(4): 1425-1437.
[13] Cui H, Mu Y, Yu L, et al. Methylation of the miR-126 gene associated with glioma progression [J]. Fam Cancer, 2016, 15(2): 317-324.

相似文献/References:

[1]吴　科　唐树军　魏剑波　黄志刚　王代文.替莫唑胺联合放疗对体外原代培养的胶质瘤细胞Ki-67表达的影响[J].中国临床神经外科杂志,2017,(05):322.[doi:10.13798/j.issn.1009-153X.2017.05.013]
　WU Ke,TANG Shu-jun,Wei Jian-bo,et al.Effect of radiotherapy combined with temozolomide on Ki-67 expression levels in primary cultured malignant glioma cells[J].,2017,(08):322.[doi:10.13798/j.issn.1009-153X.2017.05.013]
[2]张　钧　宋国智　常　成.低级别胶质瘤SLC12A5的表达及临床意义的生信分析[J].中国临床神经外科杂志,2022,27(04):269.[doi:10.13798/j.issn.1009-153X.2022.04.009]
　ZHANG Jun,SONG Guo-zhi,CHANG Cheng..Clinical meanings of SLC12A5 expression in low-grade glioma based on analysis of bioinformatics methods[J].,2022,27(08):269.[doi:10.13798/j.issn.1009-153X.2022.04.009]

备注/Memo

备注/Memo:
作者单位：450006 郑州，河南省直第三人民医院神经外科（平建峰、麻来峰、林昌福）
更新日期/Last Update: 1900-01-01