NIPSNAP1指导双重机制来抑制癌细胞的衰老
Enyi Gao1,2, Xiaoya Sun3, Rick Francis Thorne4
1Translational Research Institute, Henan Provincial People's Hospital, School of Clinical Medicine, Henan University, Zhengzhou, 450046, China.
Journal of translational medicine
|June 20, 2023
概括
这项研究确定NIPSNAP1是促进癌细胞增殖的关键调节器,通过抑制衰老来促进癌细胞的增殖. 准NIPSNAP1可能是一个新的癌症治疗策略,以诱导细胞衰老.
科学领域:
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
- 分子机制的分子机制
背景情况:
- 癌细胞在压力下逃避衰老的机制仍然不完全理解.
- 理解这些机制对于开发有效的癌症疗法至关重要.
研究的目的:
- 研究NIPSNAP1在肝细胞癌细胞增殖和衰老中的作用.
- 阐明NIPSNAP1影响癌细胞命运的分子机制.
主要方法:
- 蛋白质查和RNAi被用于识别和验证NIPSNAP1.1.
- 功能性测试包括扩散,衰老,ROS和异种移植模型.
- 通过过度表达,敲击,光酶和蛋白质酶试验来探索分子机制.
主要成果:
- NIPSNAP1促进癌细胞的增殖,并抑制衰老.
- NIPSNAP1通过隔离FBXL14稳定c-Myc,并通过SIRT3-SOD2相互作用调节活性氧物种 (ROS).
- 在体内证实NIPSNAP1的增殖和抗衰老作用.
结论:
- NIPSNAP1是c-Myc功能的关键调解者,也是细胞衰老的负调节者.
- 准NIPSNAP1是一个潜在的治疗策略,可以诱导癌细胞的衰老.
相关概念视频
Replicative Cell Senescence
3.7K
Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
3.7K
Adaptive Mechanisms in Cancer Cells
5.8K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.8K
Negative Regulator Molecules
35.5K
Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
35.5K
The Intrinsic Apoptotic Pathway
6.6K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.6K
DNA Damage can Stall the Cell Cycle
9.2K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
9.2K
Mechanisms of Retrovirus-induced Cancers
5.1K
Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
5.1K


