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科学家阐明胶质母细胞瘤患者机体肿瘤入侵扩散的分子机制

  1. 入侵
  2. 患者
  3. 扩散
  4. 机制
  5. 肿瘤
  6. 胶质母细胞瘤

来源:生物谷 2015-04-10 18:39

近日,来自达特茅斯Norris Cotton癌症研究中心的研究人员通过研究发现,转录因子Id4或许可以作为一种抑制子来抑制胶质母细胞瘤的入侵,相关研究刊登于国际杂志Oncogene上,研究者指出,我们在文章中发现Id4可以沉默基质金属蛋白酶2(MMP2)的表达,而这一作用是通过抑制对MMP2关键的Twist1蛋白来实现的。

2015年4月10日 讯 /生物谷BIOON/ --近日,来自达特茅斯Norris Cotton癌症研究中心的研究人员通过研究发现,转录因子Id4或许可以作为一种抑制子来抑制胶质母细胞瘤的入侵,相关研究刊登于国际杂志Oncogene上,研究者指出,我们在文章中发现Id4可以沉默基质金属蛋白酶2(MMP2)的表达,而这一作用是通过抑制对MMP2关键的Twist1蛋白来实现的。

研究者Israel解释道,该研究或为我们提供一种新型的治疗靶点来降低胶质母细胞瘤患者机体肿瘤细胞的入侵和扩散,而同时也提供了一种新型的生物标志物来帮助预测患者的生存情况。胶质母细胞瘤是一种致死性的原发性脑部肿瘤,肿瘤细胞往往会入侵到机体其它组织引发患者的死亡。

利用来自癌症基因组图谱(Cancer Genome Atlas)计划的书库,研究人员发现,Id4的表达和胶质母细胞瘤病人的生存直接相关联,而且和MMP2的表达存在反向关系;研究结果显示,在多形性胶质母细胞瘤中通过降低Id4的表达而引发的MMP2功能的上调或许会引发患者的发病和死亡。

靶向作用MMP基因编码的酶类的常规药物由于其存在一定的副作用,因此其在临床上并不会成功治疗患者,研究者认为,控制MMP2表达的通路蛋白或许更易于作用一种治疗靶点;而靶向作用Twist1或许可以沉默MMP2及降低肿瘤的侵袭,这或将有益于胶质母细胞瘤患者的治疗;此外Id4的表达或许也可以作为一种肿瘤生物标志物来帮助预测肿瘤入侵的程度。

本文研究表明,在肿瘤入侵中所揭示的治疗性靶点或许可以潜在地作为药物靶点,来进行胶质母细胞瘤新型疗法的开发,后期研究中研究者也希望利用Id4来作为指示胶质母细胞瘤的生物标志物,以此来预测患者机体肿瘤的扩散程度及患者的生存情况。(生物谷Bioon.com)

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"This finding suggests a novel therapeutic target to decrease invasion of tumor cells in patients and may also provide a novel biomarker that could help predict survival of patients with glioblastoma," explained Israel.
Glioblastoma is the most lethal form of primary brain tumor and leads to death in patients by invading the brain tissue in a process that allows single cells to move through normal brain tissue, which makes complete surgical removal of the tumor impossible. Israel and his team sought to understand the mechanisms that drive tumor invasion of normal tissue in glioblastoma.
Using data from The Cancer Genome Atlas (TCGA), the Dartmouth team demonstrated that Id4 expression correlates with survival of glioblastoma patients and inversely correlates with MMP2 expression. The data suggests that the upregulation of MMP2 resulting from decreased Id4 expression in glioblastoma multiforme (GBM) may contribute to the morbidity and mortality of GBM patients.
This study used Dartmouth's Shared Resources including Microscopy and Molecular Biology. "Using the core facilities greatly facilitated the conduct of the work saving time and reducing cost," Rahme said. All 14 of Dartmouth's Shared Resources are available to outside investigators by arrangement.
"Conventional drugs targeting the enzymes encoded by MMP genes have not been successful in the clinic due to adverse side effects," said Rahme. "We believe that proteins in the pathway that controls the expression of MMP2 are likely to be better therapeutic targets. Targeting Twist1 might silence MMP2 and decrease tumor invasion, which will help patients with GBM. Furthermore, the expression of Id4 may serve as a tumor biomarker that can predict the degree of tumor infiltration."
Looking forward, the therapeutic targets revealed in this study to be actors in tumor invasion need to be further characterized as drug targets and, if possible, therapeutically inhibited. Their pursuit of Id4 as a biomarker for patients with GBM continues in hopes of making useful predictions of tumor invasion and survival.

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