细胞启动因子4A-3促进质母细胞瘤的生长和通过Notch1-依赖途径的侵袭
Lei Wei1, Mika Pan2, Qiulan Jiang3
1Department of Neurology, The Fifth Affiliated Hospital of Guangxi Medical University, Nanning, 530022, Guangxi, China.
BMC cancer
|June 15, 2023
概括
细胞启动因子4A-3 (EIF4A3) 在质母细胞瘤 (GBM) 中被上调,促进瘤生长和转移. 针对EIF4A3可能为GBM治疗提供新的治疗策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 质母细胞瘤 (GBM) 是一种具有高死亡率的侵袭性脑瘤,由于其异质性.
- 细胞启动因子4A-3 (EIF4A3) 在GBM病原发生中的作用尚不清楚.
- 识别新的分子标对于改善GBM治疗结果至关重要.
研究的目的:
- 为了研究EIF4A3在质母细胞瘤中的作用.
- 为了确定EIF4A3表达在GBM患者的预后意义.
- 阐明EIF4A3介导的GBM进展背后的分子机制.
主要方法:
- 对94名GBM患者的生存分析,以将EIF4A3表达与预后相关联.
- 在体外实验中评估EIF4A3对GBM细胞增殖,迁移和入侵的影响.
- 在体内研究验证EIF4A3在GBM中的作用.
- 生物信息分析以确定EIF4A3相关的信号通路.
- RNA免疫沉以确认与Notch1.1.的相互作用.
主要成果:
- 在GBM组织中,EIF4A3表达显著上调,并与预后不佳有关.
- 抑制EIF4A3可以抑制GBM细胞的增殖,迁移和入侵.
- 过度表达EIF4A3可增强GBM细胞生长和转移潜力.
- EIF4A3参与与癌症相关的途径,包括Notch和JAK-STAT3信号传递.
- EIF4A3与Notch1相互作用,这表明它在GBM进展中的作用.
结论:
- EIF4A3是质母细胞瘤的潜在预后生物标志物.
- EIF4A3促进GBM细胞的增殖和转移.
- 诺奇1信号与EIF4A3介导的GBM进展有关,突出了一个潜在的治疗点.
相关概念视频
01:24Regulation of Angiogenesis and Blood Supply
2.6K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.6K
03:14Notch Signaling Pathway
4.3K
The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
4.3K
01:22PI3K/mTOR/AKT Signaling Pathway
3.7K
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...
3.7K
03:03mTOR Signaling and Cancer Progression
3.8K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
The mTOR pathway or the...
3.8K
01:12Role Of Notch Signalling In Intestinal Stem Cell Renewal
2.1K
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.1K