干扰素及其相关信号通路抑制脑胶质瘤侵袭的机制

doi:10.3760/cma.j.cn371439-20200601-00034

国际肿瘤学杂志 ›› 2021, Vol. 48 ›› Issue (3): 172-175.doi: 10.3760/cma.j.cn371439-20200601-00034

干扰素及其相关信号通路抑制脑胶质瘤侵袭的机制

孙彦琪, 任叶青, 郭庚^*()

山西医科大学第一医院神经外科,太原 030001

收稿日期:2020-06-01 修回日期:2020-09-30 出版日期:2021-03-08 发布日期:2021-03-25
通讯作者: 郭庚 E-mail:guogeng973@163.com
基金资助:
国家自然科学基金(81201991);中国博士后科学基金(2015M571068);中国博士后科学基金(2016T90115);山西省自然科学基金(201601D011127);山西省高等学校创新人才支持计划(晋教科)(2013-8)

Mechanism of inhibitory effect of interferon and its related signal pathway on the invasion of glioma

Sun Yanqi, Ren Yeqing, Guo Geng^*()

Department of Neurosurgery, First Hospital of Shanxi Medical University, Taiyuan 030001, China

Received:2020-06-01 Revised:2020-09-30 Online:2021-03-08 Published:2021-03-25
Contact: Guo Geng E-mail:guogeng973@163.com
Supported by:
National Natural Science Foundation of China(81201991);China Postdoctoral Science Foundation(2015M571068);China Postdoctoral Science Foundation(2016T90115);Natural Science Foundation of Shanxi Province of China(201601D011127);Program for the Outstanding Innovation Teams of Higher Learning Institutions of Shanxi Province(2013-8)

摘要/Abstract

摘要：

胶质瘤是颅内发生率较高的肿瘤,其恶性程度高、侵袭性强、致死率高等特点使目前常规治疗方法并不能达到预期的治疗效果,极大地影响患者的生命质量。干扰素作为一种具有抗增殖、抑制血管新生、抑制侵袭等作用的蛋白质,在临床中广泛应用于各种肿瘤的治疗。不少研究表明干扰素在胶质瘤的发生发展过程中起重要作用。探讨干扰素及其相关信号通路在胶质瘤侵袭过程中的作用机制,研究新的胶质瘤治疗方案在临床治疗中显得十分必要。

关键词: 胶质瘤, 侵袭, 干扰素

Abstract:

Glioma is a tumor with a high incidence of intracranial tumor. Because of its high degree of malignancy, strong invasiveness and high mortality, the current conventional treatment cannot achieve the desired therapeutic effect, which greatly affects the quality of life of patients. As a protein with the functions of anti-proliferation, anti-angiogenesis and anti-invasion, interferon is widely used in the treatment of all kinds of tumors in clinic. Many studies have shown that interferon plays an important role in the occurrence and development of gliomas. To explore the mechanism of interferon and its related signal pathway in the process of glioma invasion, and to study the new treatment of glioma is very necessary in clinical treatment.

Key words: Glioma, Invasion, Interferon

孙彦琪, 任叶青, 郭庚. 干扰素及其相关信号通路抑制脑胶质瘤侵袭的机制[J]. 国际肿瘤学杂志, 2021, 48(3): 172-175.

Sun Yanqi, Ren Yeqing, Guo Geng. Mechanism of inhibitory effect of interferon and its related signal pathway on the invasion of glioma[J]. Journal of International Oncology, 2021, 48(3): 172-175.

参考文献 29

[1]	Chen R, Smith-Cohn M, Cohen AL, et al. Glioma subclassifications and their clinical significance[J]. Neurotherapeutics, 2017,14(2):284-297. DOI: 10.1007/s13311-017-0519-x. doi: 10.1007/s13311-017-0519-x pmid: 28281173
[2]	Abrams DA, Hanson JA, Brown JM, et al. Timing of surgery and bevacizumab therapy in neurosurgical patients with recurrent high grade glioma[J]. J Clin Neurosci, 2015,22(1):35-39. DOI: 10.1016/j.jocn.2014.05.054. doi: 10.1016/j.jocn.2014.05.054 pmid: 25481268
[3]	Castro F, Cardoso AP, Gonçalves RM, et al. Interferon-gamma at the crossroads of tumor immune surveillance or evasion[J]. Front Immunol, 2018,9:847. DOI: 10.3389/fimmu.2018.00847. doi: 10.3389/fimmu.2018.00847 pmid: 29780381
[4]	Yokota A, Hirai H, Sato R, et al. C/EBPβ is a critical mediator of IFN-α-induced exhaustion of chronic myeloid leukemia stem cells[J]. Blood Adv, 2019,3(3):476-488. DOI: 10.1182/bloodadvances.2018020503. pmid: 30755436
[5]	Lohmann B, Le Rhun E, Silginer M, et al. nterferon-β sensitizes human glioblastoma cells to the cyclin-dependent kinase inhibitor, TG02[J]. Oncol Lett, 2020,19(4):2649-2656. DOI: 10.3892/ol.2020.11362. doi: 10.3892/ol.2020.11362 pmid: 32218815
[6]	Medrano RFV, Hunger A, Mendonça SA, et al. Immunomodulatory and antitumor effects of type Ⅰ interferons and their application in cancer therapy[J]. Oncotarget, 2017,8(41):71249-71284. DOI: 10.18632/oncotarget.19531. doi: 10.18632/oncotarget.19531 pmid: 29050360
[7]	Swiatek-Machado K, Kaminska B. STAT signaling in glioma cells[J]. Adv Exp Med Biol, 2020,1202:203-222. DOI: 10.1007/978-3-030-30651-9_10. pmid: 32034715
[8]	Zhang Y, Liu Z. STAT1 in cancer: friend or foe?[J]. Discov Med, 2017,24(130):19-29. pmid: 28950072
[9]	Hua L, Wang G, Wang Z, et al. Activation of STAT1 by the FRK tyrosine kinase is associated with human glioma growth[J]. J Neurooncol, 2019,143(1):35-47. DOI: 10.1007/s11060-019-03143-w. doi: 10.1007/s11060-019-03143-w pmid: 30993511
[10]	Zhang Y, Jin G, Zhang J, et al. Overexpression of STAT1 suppresses angiogenesis under hypoxia by regulating VEGF A in human glioma cells[J]. Biomed Pharmacother, 2018,104:566-575. DOI: 10.1016/j.biopha.2018.05.079. doi: 10.1016/j.biopha.2018.05.079 pmid: 29800921
[11]	Arslan AD, Sassano A, Saleiro D, et al. Human SLFN5 is a transcriptional co-repressor of STAT1-mediated interferon responses and promotes the malignant phenotype in glioblastoma[J]. Oncogene, 2017,36(43):6006-6019. DOI: 10.1038/onc.2017.205. doi: 10.1038/onc.2017.205 pmid: 28671669
[12]	Rupaimoole R, Slack FJ. MicroRNA therapeutics: towards a new era for the management of cancer and other diseases[J]. Nat Rev Drug Discov, 2017,16(3):203-222. DOI: 10.1038/nrd.2016.246. doi: 10.1038/nrd.2016.246 pmid: 28209991
[13]	Chen J, Zhong Y, Li L. miR-124 and miR-203 synergistically inactivate EMT pathway via coregulation of ZEB2 in clear cell renal cell carcinoma (ccRCC)[J]. J Transl Med, 2020,18(1):69. DOI: 10.1186/s12967-020-02242-x. doi: 10.1186/s12967-020-02242-x pmid: 32046742
[14]	Yang CH, Wang Y, Sims M, et al. MiRNA203 suppresses the expression of protumorigenic STAT1 in glioblastoma to inhibit tumorigenesis[J]. Oncotarget, 2016,7(51):84017-84029. DOI: 10.18632/oncotarget.12401. doi: 10.18632/oncotarget.12401 pmid: 27705947
[15]	Zhou P, Jiang N, Zhang GX, et al. MiR-203 inhibits tumor invasion and metastasis in gastric cancer by ATM.[J]. Acta Biochim Biophys Sin (Shanghai), 2016,48(8):696-703. DOI: 10.1093/abbs/gmw063. doi: 10.1093/abbs/gmw063
[16]	Yang CH, Wang Y, Sims M, et al. MicroRNA203a suppresses glioma tumorigenesis through an ATM-dependent interferon response pathway[J]. Oncotarget, 2017,8(68):112980-112991. DOI: 10.18632/oncotarget.22945. doi: 10.18632/oncotarget.22945 pmid: 29348882
[17]	Zhang J, Zhu ZQ, Li YX, et al. Tim-3 expression in glioma cells is associated with drug resistance[J]. J Cancer Res Ther, 2019,15(4):882-888. DOI: 10.4103/jcrt.JCRT_630_18. doi: 10.4103/jcrt.JCRT_630_18 pmid: 31436247
[18]	Liu Z, Han H, He X, et al. Expression of the galectin-9-Tim-3 pathway in glioma tissues is associated with the clinical manifestations of glioma[J]. Oncol Lett, 2016,11(3):1829-1834. DOI: 10.3892/ol.2016.4142. pmid: 26998085
[19]	Li X, Wang B, Gu L, et al. Tim-3 expression predicts the abnormal innate immune status and poor prognosis of glioma patients[J]. Clin Chim Acta, 2018,476:178-184. DOI: 10.1016/j.cca.2017.11.022. doi: 10.1016/j.cca.2017.11.022 pmid: 29174343
[20]	Hannen R, Bartsch JW. Essential roles of telomerase reverse transcriptase hTERT in cancer stemness and metastasis[J]. FEBS Lett, 2018,592(12):2023-2031. DOI: 10.1002/1873-3468.13084. doi: 10.1002/1873-3468.13084 pmid: 29749098
[21]	Li G, Shen J, Cao J, et al. Alternative splicing of human telomerase reverse transcriptase in gliomas and its modulation mediated by CX-5461[J]. J Exp Clin Cancer Res, 2018,37(1):78. DOI: 10.1186/s13046-018-0749-8. doi: 10.1186/s13046-018-0749-8 pmid: 29631594
[22]	George J, Banik NL, Ray SK. Knockdown of hTERT and concurrent treatment with interferon-gamma inhibited proliferation and invasion of human glioblastoma cell lines[J]. Int J Biochem Cell Biol, 2010,42(7):1164-1173. DOI: 10.1016/j.biocel.2010.04.002. doi: 10.1016/j.biocel.2010.04.002 pmid: 20394835
[23]	Sun G, Wang Y, Zhang J, et al. MiR-15b/HOTAIR/p53 form a regulatory loop that affects the growth of glioma cells[J]. J Cell Biochem, 2018,119(6):4540-4547. DOI: 10.1002/jcb.26591. pmid: 29323737
[24]	Sarma PP, Dutta D, Mirza Z, et al. [Point mutations in the DNA binding domain of p53 contribute to glioma progression and poor prognosis][J]. Mol Biol (Mosk), 2017,51(2):334-341. DOI: 10.7868/S0026898417020185.
[25]	Shen D, Guo CC, Wang J, et al. Interferon-α/β enhances temozolomide activity against MGMT-positive glioma stem-like cells[J]. Oncol Rep, 2015,34(5):2715-2721. DOI: 10.3892/or.2015.4232. doi: 10.3892/or.2015.4232 pmid: 26329778
[26]	Jiapaer S, Furuta T, Tanaka S, et al. Potential strategies overcoming the temozolomide resistance for glioblastoma[J]. Neurol Med Chir (Tokyo), 2018,58(10):405-421. DOI: 10.2176/nmc.ra.2018-0141. doi: 10.2176/nmc.ra.2018-0141
[27]	GuhaSarkar D, Neiswender J, Su Q, et al. Intracranial AAV-IFN-β gene therapy eliminates invasive xenograft glioblastoma and improves survival in orthotopic syngeneic murine model[J]. Mol Oncol, 2017,11(2):180-193. DOI: 10.1002/1878-0261.12020. doi: 10.1002/1878-0261.12020 pmid: 28098415
[28]	Pu W, Qiu J, Riggins GJ, et al. Matrix protease production, epithelial-to-mesenchymal transition marker expression and invasion of glioblastoma cells in response to osmotic or hydrostatic pressure[J]. Sci Rep, 2020,10(1):2634. DOI: 10.1038/s41598-020-59462-w. doi: 10.1038/s41598-020-59462-w pmid: 32060379
[29]	Wang H, Hou Y, Hu Y, et al. Enzyme-activatable interferon-poly(α-amino acid) conjugates for tumor microenvironment potentiation[J]. Biomacromolecules, 2019,20(8):3000-3008. DOI: 10.1021/acs.biomac.9b00560. pmid: 31310511

干扰素及其相关信号通路抑制脑胶质瘤侵袭的机制

Mechanism of inhibitory effect of interferon and its related signal pathway on the invasion of glioma

RichHTML

PDF

可视化

摘要/Abstract

引用本文

使用本文

参考文献 29

相关文章 15

编辑推荐

Metrics

本文评价

[1]	刘萍萍, 何学芳, 张翼, 杨旭, 张珊珊, 季一飞. 原发性脑胶质瘤患者术后复发危险因素及预测模型构建[J]. 国际肿瘤学杂志, 2024, 51(4): 193-197.
[2]	邢明泉, 葛洪峰, 张丽侠, 韩浩, 吴维霞. 疑似免疫性血小板减少症的侵袭性自然杀伤细胞白血病1例[J]. 国际肿瘤学杂志, 2023, 50(5): 318-320.
[3]	张子叔, 乌新林. 肿瘤微环境中乳酸的作用机制及相关治疗[J]. 国际肿瘤学杂志, 2022, 49(6): 349-352.
[4]	肖楠, 孙鹏飞. 氧化应激在胶质瘤放化疗敏感性中的研究进展[J]. 国际肿瘤学杂志, 2022, 49(6): 357-361.
[5]	石雨, 陈曦, 许梦琪, 张滢滢, 冀洪海, 蒋英英. 沉默PSIP1基因对口腔鳞状细胞癌细胞迁移及侵袭的影响[J]. 国际肿瘤学杂志, 2022, 49(3): 129-133.
[6]	朱一硕, 崔玉洁, 刘崎, 李军, 范月超. 脑胶质瘤患者术后早期复发危险因素分析及预测模型构建[J]. 国际肿瘤学杂志, 2022, 49(2): 79-83.
[7]	孔春禹, 孙鹏飞. SLC7A11与胶质瘤[J]. 国际肿瘤学杂志, 2022, 49(10): 604-607.
[8]	郭世豪, 任叶青, 郭庚. 脑胶质瘤血管生成拟态分子机制[J]. 国际肿瘤学杂志, 2021, 48(6): 362-365.
[9]	王宪伟, 史美燕, 王凤芹, 齐福, 王朝喆, 周飞. TSA上调miR-4298靶向抑制PADI4表达在诱导U251细胞凋亡中的作用[J]. 国际肿瘤学杂志, 2021, 48(4): 193-199.
[10]	张雯, 胡伟国, 宋启斌. 3D-ASL与DCE-MRI在脑胶质瘤复发与放射性脑坏死鉴别诊断中的价值[J]. 国际肿瘤学杂志, 2021, 48(10): 631-634.
[11]	王宁菊, 陈冬梅, 章恒, 胡萍, 王燕. 靶向沉默PRL-3基因对肺癌细胞增殖、迁移、侵袭及上皮间质转化的影响[J]. 国际肿瘤学杂志, 2021, 48(1): 18-23.
[12]	魏梦雨, 马力. Mfn2在肿瘤中的研究进展[J]. 国际肿瘤学杂志, 2021, 48(1): 45-47.
[13]	李钰祥, 王新文. 干扰素治疗肿瘤相关的信号通路及临床应用[J]. 国际肿瘤学杂志, 2020, 47(6): 364-367.
[14]	赵聪选, 于韬. 胶质瘤相关基因的挖掘及预测[J]. 国际肿瘤学杂志, 2020, 47(5): 293-296.
[15]	南阳, 钟跃. 长非编码RNA在神经胶质瘤研究中的新进展[J]. 国际肿瘤学杂志, 2020, 47(2): 98-102.