在癌症的双重向治疗中向希斯脱糖酶6的向
Milan Beljkas1, Aleksandra Ilic1, Alen Cebzan1
1Faculty of Pharmacy, Department of Pharmaceutical Chemistry, University of Belgrade, Vojvode Stepe 450, 11221 Belgrade, Serbia.
Pharmaceutics
|November 25, 2023
概括
双标HDAC6抑制剂通过克服单标药物的局限性,在癌症治疗方面表现有前途. 本综述探讨了双标HDAC6抑制剂的进展,以提高癌症治疗疗效和减少副作用.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 在瘤学瘤学.
背景情况:
- 基因组脱乙酶 (HDACs) 调节蛋白质乙化.
- 具体而言,HDAC6对非质蛋白的乙化有影响,其过度表达与各种癌症有关.
- 目前的选择性HDAC6抑制剂面临的挑战是有效性和非目标效应.
研究的目的:
- 审查用于癌症治疗的双标HDAC6抑制剂的发展.
- 突出克服现有HDAC6抑制剂的局限性的策略.
- 讨论双重向方法在瘤学的潜力.
主要方法:
- 对HDAC6抑制剂研究的文献综述.
- 对结合HDAC6抑制与其他机制的双重目标策略的分析.
- 评估新型双重标化合物的疗效和特异性.
主要成果:
- 双标的HDAC6抑制剂旨在提高抗癌疗效.
- 这些抑制剂可以减少非目标效应并改善治疗结果.
- 新趋势侧重于将HDAC6抑制与其他向癌症的策略相结合.
结论:
- 双位HDAC6抑制剂代表了癌症的有前途的治疗策略.
- 需要进一步的研究来优化临床应用的双抑制剂.
- 这种方法有可能为更有效,更安全的癌症治疗提供潜力.
相关概念视频
Targeted Cancer Therapies
7.6K
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...
7.6K
Spreading of Chromatin Modifications
8.3K
The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
The writer...
Writers
The writer...
8.3K
Histone Variants at the Centromere
4.3K
Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3...
4.3K
Abnormal Proliferation
4.5K
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...
4.5K
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
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


