相关实验视频
Updated: Jul 1, 2025

The Soft Agar Colony Formation Assay
Published on: October 27, 2014
TRIM67通过通过DLK1的Ubiquitination积极调节Notch Pathway促进非小细胞肺癌的发展
Jun Jiang1, Xinjie Dong1, Jixuan Liu1
1Department of Pathology, Lequn Branch, The First Hospital of Jilin University, Changchun, China.
含三部分动图67 (TRIM67) 通过激活Notch通路,促进非小细胞肺癌 (NSCLC) 的生长. TRIM67在DLK1上无处不在,增强癌细胞的入侵,迁移和增殖,表明潜在的治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 含有三方基因的67 (TRIM67) 是一种E3泛基因酶,涉及致癌.
- 以前的研究将TRIM67表达与晚期瘤阶段,转移和各种癌症的不良预后联系起来.
- 已经证明TRIM67可以激活Notch路径,促进癌细胞的攻击性.
研究的目的:
- 阐明TRIM67在非小细胞肺癌 (NSCLC) 中影响Notch路径的特定机制.
- 研究TRIM67在调节DLK1中的作用及其随后对NSCLC细胞行为的影响.
主要方法:
- 免疫组织化学评估TRIM67表达及其与临床病理特征的相关性.
- 西方涂抹和无处不在测试以确定TRIM67对DLK1.1的影响.
- 细胞测定 (入侵,迁移,增殖) 以评估TRIM67-DLK1相互作用的功能后果.
主要成果:
- TRIM67表达与NSCLC的预后不佳指标相关,包括p-TNM阶段和淋巴结转移.
- 通过其RING域,TRIM67通过其RING域直接在非正规的Notch配方1 (DLK1) 和非正规的Notch配方1 (DLK1) 等非典型的配方三角体中无处不在.
- 这种TRIM67的无处不在事件导致了Notch路径的激活,促进NSCLC细胞的入侵,迁移和增殖.
结论:
- TRIM67通过无处不在的DLK1和激活Notch信号通路来促进NSCLC的进展.
- TRIM67代表了管理NSCLC的潜在治疗标.
- 针对TRIM67-DLK1-Notch轴可能为NSCLC治疗提供一种新的策略.
更多相关视频
09:08Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
Published on: January 12, 2020
06:51Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
Published on: July 21, 2018
相关概念视频
Notch Signaling Pathway
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...
Role Of Notch Signalling In Intestinal Stem Cell Renewal
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...
Abnormal Proliferation
Canonical Wnt Signaling Pathway
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
lncRNA - Long Non-coding RNAs