基于生物信息学的分析显示,CYTL1的升高是BRAF突变黑色素瘤的潜在治疗标
Lei Tao1, Yingyue Cui2, Jiarui Sun2
1Nanjing Institute for Food and Drug Control, Nanjing, China.
Frontiers in cell and developmental biology
|September 25, 2023
概括
研究人员确定CYTL1是黑色素瘤的有希望的治疗点,特别是BRAF突变黑色素瘤. 高CYTL1表达与预后较差和细胞迁移增加相关,这表明它在黑色素瘤进展中的作用.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 尽管治疗方面取得了进展,但黑色素瘤的预后仍然很差.
- 在黑色素瘤中,BRAF突变很常见,导致疾病的进展.
- 了解黑色素瘤的潜在机制对于开发新疗法至关重要.
研究的目的:
- 为了确定BRAF突变黑色素瘤的新型治疗点.
- 研究CYTL1在黑色素瘤进展和预后中的作用.
- 探索CYTL1作为潜在的预后生物标志物和治疗点.
主要方法:
- 使用TCGA和GEO数据库分析了黑色素瘤与正常组织中的差异表达基因 (DEG),以及BRAF突变与野生型黑色素瘤之间的差异表达基因.
- 评估CYTL1表达,与临床结果 (OS,DFS) 的相关性,以及相关的信号通路.
- 进行了体外实验 (CCK8,Transwell,迁移试验) 来评估CYTL1对黑色素瘤细胞行为的打击的影响.
主要成果:
- 确定了24个重叠的DEG,其中CYTL1在黑色素瘤中表达高,特别是BRAF突变型.
- 高CYTL1表达与上皮细胞-介质细胞过渡 (EMT),细胞周期,紫外线反应以及较差的整体存活率 (OS) 和无病存活率 (DFS) 相相关.
- 在体外,CYTL1的敲除显著抑制了黑色素瘤细胞迁移和侵入.
结论:
- CYTL1是黑色素瘤的一个有价值的预后生物标志物.
- CYTL1代表了一个潜在的治疗点,特别是在BRAF突变黑色素瘤中.
- 准CYTL1可能为改善黑色素瘤治疗结果提供了一种新策略.
更多相关视频
06:25Author Spotlight: Assessing the Potential of Circulating Tumor Cells in Leptomeningeal Disease Research
Published on: March 29, 2024
916
07:42Assessment of Resistance to Tyrosine Kinase Inhibitors by an Interrogation of Signal Transduction Pathways by Antibody Arrays
Published on: September 19, 2018
8.0K
相关概念视频
Targeted Cancer Therapies
7.7K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
There are several types of targeted therapies against...
7.7K
Abnormal Proliferation
4.6K
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...
4.6K
Combination Therapies and Personalized Medicine
4.9K
Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
4.9K
mTOR 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
M-Cdk Drives Transition Into Mitosis
5.6K
Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
5.6K
Inhibition of Cdk Activity
4.8K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.8K
