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胶质母细胞瘤中细胞受体激活的治疗潜力进展

Advances on the therapeutic potential of cell receptor activation in glioblastoma.

作者信息

Contreras-Chávez Gerson G, Zapi-Colin Luis A, Estrada José A, Contreras Irazú, Estrada José A

机构信息

Neurochemistry Laboratory, Faculty of Medicine, Universidad Autónoma del Estado de México, Toluca, México.

Neurochemistry Laboratory, Faculty of Medicine, Universidad Autónoma del Estado de México, Paseo Tollocan esq. Jesús Carranza s/n, Colonia Moderna de la Cruz, Toluca, C.P. 50180, México.

出版信息

Mol Biol Rep. 2025 Feb 5;52(1):207. doi: 10.1007/s11033-025-10312-w.

DOI:10.1007/s11033-025-10312-w
PMID:39907852
Abstract

Glioblastoma multiforme is the most common and aggressive malignant brain tumor. Current therapies have been unable to improve life expectancy in patients. This cancer is frequently accompanied by overexpression of receptors, such as EGFR, VEGFR and TLRs, involved in the regulation of inflammation, cell proliferation, differentiation, and survival. The present review summarizes current knowledge from preclinical and clinical studies investigating the role of pattern recognition and tyrosine kinase receptors in glioblastoma development and evolution, and their possible use to improve treatment outcomes and patient survival.

摘要

多形性胶质母细胞瘤是最常见且侵袭性最强的恶性脑肿瘤。目前的治疗方法未能提高患者的预期寿命。这种癌症常伴有受体的过表达,如表皮生长因子受体(EGFR)、血管内皮生长因子受体(VEGFR)和Toll样受体(TLRs),这些受体参与炎症、细胞增殖、分化和存活的调节。本综述总结了临床前和临床研究的现有知识,这些研究探讨了模式识别受体和酪氨酸激酶受体在胶质母细胞瘤发生发展中的作用,以及它们在改善治疗效果和患者生存率方面的潜在用途。

相似文献

1
Advances on the therapeutic potential of cell receptor activation in glioblastoma.胶质母细胞瘤中细胞受体激活的治疗潜力进展
Mol Biol Rep. 2025 Feb 5;52(1):207. doi: 10.1007/s11033-025-10312-w.
2
Advances in Targeting the Epidermal Growth Factor Receptor Pathway by Synthetic Products and Its Regulation by Epigenetic Modulators As a Therapy for Glioblastoma.表皮生长因子受体通路的靶向治疗:合成产物的进展及其作为胶质母细胞瘤治疗方法的表观遗传调节剂的调控。
Cells. 2019 Apr 12;8(4):350. doi: 10.3390/cells8040350.
3
Chronic activation of wild-type epidermal growth factor receptor and loss of Cdkn2a cause mouse glioblastoma formation.野生型表皮生长因子受体的慢性激活和 Cdkn2a 的缺失导致小鼠脑胶质瘤的形成。
Cancer Res. 2011 Dec 1;71(23):7198-206. doi: 10.1158/0008-5472.CAN-11-1514. Epub 2011 Oct 10.
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Targeting ErbB receptors in high-grade glioma.靶向高级别神经胶质瘤中的 ErbB 受体。
Curr Pharm Des. 2011;17(23):2468-87. doi: 10.2174/138161211797249233.
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Differentiation of glioblastoma multiforme stem-like cells leads to downregulation of EGFR and EGFRvIII and decreased tumorigenic and stem-like cell potential.多形性胶质母细胞瘤干细胞样细胞的分化导致表皮生长因子受体(EGFR)和EGFRvIII的下调,并降低致瘤性和干细胞样细胞潜能。
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An LXR agonist promotes glioblastoma cell death through inhibition of an EGFR/AKT/SREBP-1/LDLR-dependent pathway.配体 X 受体激动剂通过抑制 EGFR/AKT/SREBP-1/LDLR 依赖性途径促进胶质母细胞瘤细胞死亡。
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Deregulated signaling pathways in glioblastoma multiforme: molecular mechanisms and therapeutic targets.胶质母细胞瘤中失调的信号通路:分子机制与治疗靶点。
Cancer Invest. 2012 Jan;30(1):48-56. doi: 10.3109/07357907.2011.630050.
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MicroRNAs involved in the EGFR pathway in glioblastoma.胶质母细胞瘤中涉及 EGFR 通路的 microRNAs。
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VEGFR inhibitors upregulate CXCR4 in VEGF receptor-expressing glioblastoma in a TGFβR signaling-dependent manner.血管内皮生长因子受体(VEGFR)抑制剂以转化生长因子β受体(TGFβR)信号依赖的方式上调表达VEGF受体的胶质母细胞瘤中的CXCR4。
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Erlotinib resistance in EGFR-amplified glioblastoma cells is associated with upregulation of EGFRvIII and PI3Kp110δ.表皮生长因子受体(EGFR)扩增型胶质母细胞瘤细胞对厄洛替尼的耐药性与 EGFRvIII 和 PI3Kp110δ 的上调有关。
Neuro Oncol. 2013 Oct;15(10):1289-301. doi: 10.1093/neuonc/not093. Epub 2013 Jul 21.

本文引用的文献

1
Correlation of LLT-1 and NLRC4 inflammasome and its effect on glioblastoma prognosis.LLT-1 和 NLRC4 炎性小体的相关性及其对胶质母细胞瘤预后的影响。
J Neurooncol. 2024 Sep;169(3):543-553. doi: 10.1007/s11060-024-04750-y. Epub 2024 Jun 22.
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Resveratrol ameliorates glioblastoma inflammatory response by reducing NLRP3 inflammasome activation through inhibition of the JAK2/STAT3 pathway.白藜芦醇通过抑制 JAK2/STAT3 通路减少 NLRP3 炎性小体激活,从而改善神经胶质瘤的炎症反应。
J Cancer Res Clin Oncol. 2024 Mar 28;150(3):168. doi: 10.1007/s00432-024-05625-5.
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Signaling Pathways of AXL Receptor Tyrosine Kinase Contribute to the Pathogenetic Mechanisms of Glioblastoma.
AXL 受体酪氨酸激酶信号通路参与胶质母细胞瘤的发病机制。
Cells. 2024 Feb 19;13(4):361. doi: 10.3390/cells13040361.
4
Preclinical and early clinical studies of a novel compound SYHA1813 that efficiently crosses the blood-brain barrier and exhibits potent activity against glioblastoma.新型化合物SYHA1813的临床前和早期临床研究,该化合物能有效穿过血脑屏障并对胶质母细胞瘤表现出强效活性。
Acta Pharm Sin B. 2023 Dec;13(12):4748-4764. doi: 10.1016/j.apsb.2023.09.009. Epub 2023 Sep 22.
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In vivo antiangiogenic effect of nimbolide, trans-chalcone and piperine for use against glioblastoma.尼莫内酯、反式查尔酮和胡椒碱的体内抗血管生成作用及其在神经胶质瘤治疗中的应用。
BMC Cancer. 2023 Nov 30;23(1):1173. doi: 10.1186/s12885-023-11625-4.
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NLRP6 potentiates PI3K/AKT signalling by promoting autophagic degradation of p85α to drive tumorigenesis.NLRP6 通过促进 p85α 的自噬降解来增强 PI3K/AKT 信号传导,从而驱动肿瘤发生。
Nat Commun. 2023 Sep 28;14(1):6069. doi: 10.1038/s41467-023-41739-z.
7
A novel FGFR1 inhibitor CYY292 suppresses tumor progression, invasion, and metastasis of glioblastoma by inhibiting the Akt/GSK3β/snail signaling axis.一种新型FGFR1抑制剂CYY292通过抑制Akt/GSK3β/蜗牛信号轴来抑制胶质母细胞瘤的肿瘤进展、侵袭和转移。
Genes Dis. 2023 Apr 3;11(1):479-494. doi: 10.1016/j.gendis.2023.02.035. eCollection 2024 Jan.
8
The IL13α 2R paves the way for anti-glioma nanotherapy.白细胞介素13α2受体为抗胶质瘤纳米治疗铺平了道路。
Genes Dis. 2021 Sep 15;10(1):89-100. doi: 10.1016/j.gendis.2021.08.006. eCollection 2023 Jan.
9
A phase I dose-escalation study of SYHA1813, a VEGFR and CSF1R inhibitor, in patients with recurrent High-Grade Gliomas or Advanced Solid Tumors.SYHA1813 是一种血管内皮生长因子受体(VEGFR)和集落刺激因子 1 受体(CSF1R)抑制剂的 I 期剂量递增研究,该药物用于治疗复发性高级别脑胶质瘤或晚期实体瘤患者。
Invest New Drugs. 2023 Apr;41(2):296-305. doi: 10.1007/s10637-022-01325-4. Epub 2023 Mar 8.
10
Nucleotide-Binding Oligomerization Domain (NOD)-Like Receptor Subfamily C (NLRC) as a Prognostic Biomarker for Glioblastoma Multiforme Linked to Tumor Microenvironment: A Bioinformatics, Immunohistochemistry, and Machine Learning-Based Study.核苷酸结合寡聚化结构域(NOD)样受体C亚家族(NLRC)作为与肿瘤微环境相关的多形性胶质母细胞瘤的预后生物标志物:一项基于生物信息学、免疫组织化学和机器学习的研究
J Inflamm Res. 2023 Feb 10;16:523-537. doi: 10.2147/JIR.S397305. eCollection 2023.