揭示蛋白质翻译后修改在结质瘤预后中的作用
Zhipeng Jiang1,2,3, Hanxue Huang4,5, Youwei Guo1,2,3
1Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, P.R. China.
CNS neuroscience & therapeutics
|March 16, 2025
概括
这项研究揭示了翻译后修改 (PTMs) 如何推动质瘤的进展. 准TOM1L1,一个关键蛋白质,为治疗侵略性脑瘤提供了新的希望.
科学领域:
- 神经瘤学神经瘤学
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 质瘤是一种侵略性的中枢神经系统恶性瘤.
- 翻译后修饰 (PTMs) 关键调节瘤性过程.
- 在质瘤进展中缺乏PTM的系统性表征.
研究的目的:
- 揭示质瘤进展的分子机制,重点关注PTMs.
- 为了识别PTM驱动的质瘤分子亚型.
- 为了开发一种质瘤的预后模型.
主要方法:
- 用于患者聚类的PTM通路分析.
- 临床结果,突变和免疫微环境的比较分析.
- 机器学习用于使用差异表达基因 (DEG) 构建预后预测模型.
- 在体外验证TOM1L1在质瘤中的作用.
主要成果:
- PTMs显著影响质瘤的预后,氨和氨的调节失调与侵略性特征相关.
- 包括TOM1L1在内的预后模型显示出高预测准确度 (c指数=0.867).
- 在体外实验证实TOM1L1通过调节PTM通路促进恶性进展.
结论:
- 这项研究提出了第一个全面的PTM图谱在质瘤中,识别了具有临床影响的亚型特定模式.
- TOM1L1是一个有前途的预后生物标志物和潜在的治疗标.
- 准PTM通路为质瘤提供了新的治疗策略.
更多相关视频
05:45Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections
Published on: July 31, 2017
9.6K
09:40Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
5.6K
相关概念视频
Covalently Linked Protein Regulators
6.7K
Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein....
These groups modify specific amino acids in a protein....
6.7K
Protein Glycosylation
6.6K
Glycosylation, the most common post-translational modification for proteins, serves diverse functions. Adding sugars to proteins makes the proteins more resistant to proteolytic digestion. Glycosylated proteins can act as markers and receptors to promote cell-cell adhesion. Additionally, they have many essential quality control functions in the cell, such as correct protein folding and facilitating transport of misfolded proteins to the cytosol, which can be degraded.
Glycosylation occurs in...
Glycosylation occurs in...
6.6K
mTOR Signaling and Cancer Progression
3.7K
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...
3.7K
PI3K/mTOR/AKT Signaling Pathway
3.4K
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...
3.4K
Protein Modifications in the RER
5.0K
Modification of secretory and transmembrane proteins entering the rough ER begins in the ER lumen. These modifications aid in protein folding and stabilize the acquired tertiary structure. Protein modifications in the rough ER co-occur at different stages of protein folding.
Broadly, these modifications can be categorized into four main categories — glycosylation, formation of disulfide bonds, assembly of protein subunits, and specific proteolytic cleavages like removal of signal...
Broadly, these modifications can be categorized into four main categories — glycosylation, formation of disulfide bonds, assembly of protein subunits, and specific proteolytic cleavages like removal of signal...
5.0K
Abnormal Proliferation
4.4K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.4K
