[1]杨覃,肖虹.HCG11通过调控miR-4425/FDFT1通路对脑胶质瘤细胞的恶性进展的作用机制研究[J].卒中与神经疾病杂志,2024,(01):63-72.[doi:10.3969/j.issn.1007-0478.2024.01.011]
　Yang Qin,Xiao Hong..Effects of HCG11 on malignant progression of glioma cells by regulating miR-4425/FDFT1 pathway[J].Stroke and Nervous Diseases,2024,(01):63-72.[doi:10.3969/j.issn.1007-0478.2024.01.011]
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HCG11通过调控miR-4425/FDFT1通路对脑胶质瘤细胞的恶性进展的作用机制研究()
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《卒中与神经疾病》杂志[ISSN:1007-0478/CN:42-1402/R]

卷:
期数:
2024年01期
页码:
63-72
栏目:
论著
出版日期:
2024-02-20

文章信息/Info

Title:
Effects of HCG11 on malignant progression of glioma cells by regulating miR-4425/FDFT1 pathway
文章编号:
1007-0478(2024)01-0063-10
作者:
杨覃; 肖虹
401144 重庆两江新区第一人民医院神经外科\[杨覃 肖虹（通信作者）\]
Author(s):
Yang Qin;  Xiao Hong.
Department of neurosurgery, Chongqing Liangjiang New Area First Peoples Hospital, Chongqing 401144
关键词:
人白细胞抗原复合物11; 微小RNA-4425; 法呢基二磷酸酯法呢基转移酶1; 脑胶质瘤; 细胞增殖; 细胞凋亡; 化疗耐药
Keywords:
HCG11 MiR-4425 FDFT1 Glioma Cell proliferation Apoptosis Chemoresistance
分类号:
Q253 R739.41
DOI:
10.3969/j.issn.1007-0478.2024.01.011
文献标志码:
A
摘要:
目的 研究长链非编码RNA（Long non-coding RNA，LncRNA）人白细胞抗原复合物11（Human leukocyte antigen complex group 11，HCG11）通过微小RNA（Micro RNA，miR）-4425/法呢基二磷酸酯法呢基转移酶1（Farnesyl-diphosphate farnesyltransferase 1，FDFT1）轴抑制脑胶质瘤细胞恶性进展的作用和分子机制。 方法 收集本院脑胶质瘤患者的肿瘤组织及邻近的正常组织，并通过实时荧光定量聚合酶链反应（Real-time quantitative reverse transcription polymerase chain reaction，qRT-PCR）技术检测HCG11，miR-4425和FDFT1的表达水平；构建替莫唑胺耐药株，并通过细胞计数试剂盒8（Cell counting kit 8，CCK-8）实验和流式细胞术检测空白对照组（pcDNA-negtive control，pcDNA-NC）、过表达HCG11组（Over expression of pc-HCG11，pc-HCG11）、过表达miR-4425类似物组（Over expression of miR-4425 mimics，miR-4425 mimics）的细胞活力和凋亡情况；通过免疫印迹技术和双荧光素酶报告基因系统检测各组细胞的FDFT1蛋白表达水平和HCG11，miR-4425，FDFT1之间的靶向关系。 结果 HCG11在脑胶质瘤组织和细胞系中低表达；过表达HCG11可抑制脑胶质瘤细胞的恶性增殖并促进凋亡；过表达HCG11能促进脑胶质瘤细胞的化疗敏感性；HCG11直接靶向并负向调控miR-4425表达；miR-4425通过靶向3′端非翻译区（3′Untranslated regions，3′UTR）负向调控FDFT1；HCG11通过miR-4425调控FDFT1表达并促进脑胶质瘤细胞的化疗敏感。 结论 HCG11通过负向调控miR-4425以增加其靶蛋白FDFT1表达，从而抑制脑胶质瘤细胞增殖并促进细胞凋亡，并最终提高化疗的敏感性。
Abstract:
Objective〖WTBZ〗 To study the inhibitory effect of long noncoding RNA HCG11 on the malignant progression of glioma cells through the miR-4425/FDFT1 axis and its molecular mechanism. 〖WTHZ〗Methods 〖WTBZ〗 Tumor tissues and adjacent normal tissues of glioma patients were collected from our hospital, and the expression levels of HCG11, miR-4425 and FDFT1 were detected by real-time quantitative PCR. Temozolomid-resistant strains were constructed, and the effects of pcDNA-NC, pc-HCG11 and miR-4425 mimics on cell vitality and apoptosis in each group were detected by CCK-8 assay and flow cytometry. Western blotting and a dual luciferase reporter system were used to detect the expression of FDFT1 protein and the targeting relationship among HCG11, miR-4425 and FDFT1. 〖WTHZ〗Results 〖WTBZ〗 The expression of HCG11 was low in glioma tissues and cell lines. Overexpression of HCG11 inhibited malignant proliferation and promoted apoptosis of glioma cells. HCG11 overexpression promoted the sensitivity of glioma cells to chemotherapy. HCG11 directly targeted and negatively regulated miR-4425, and miR-4425 negatively regulated FDFT1 by targeting the 3′UTR. HCG11 regulated FDFT1 through miR-4425 and promoted the chemotherapeutic sensitivity of glioma cells. 〖WTHZ〗Conclusion 〖WTBZ〗 HCG11 negatively regulates miR-4425 to increase the expression level of its target protein FDFT1, thereby inhibiting the proliferation of glioma cells and promoting cell apoptosis and ultimately improving the sensitivity of chemotherapy.

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更新日期/Last Update: 2024-02-20