局部和细胞内在补充:癌症进展中的新参与者
1INSERM, UMR_S 1138, Centre de Recherche des Cordeliers, Sorbonne Universités, Université de Paris, Paris, France.
Seminars in immunology
|June 25, 2025
概括
补体系统在癌症中起着双重作用,抑制瘤,同时促进生长和扩散. 新的研究揭示了其令人惊的细胞内功能,影响癌症的进展和治疗耐药性.
科学领域:
- 免疫学 免疫学 免疫学
- 在瘤学瘤学.
背景情况:
- 补体系统是天生的免疫系统的关键部分.
- 传统上,它在癌症中的作用被认为是细胞外的,具有作为瘤抑制剂和促进剂的双重功能.
- 新出现的证据表明,瘤进展中非正规的细胞内作用.
研究的目的:
- 探索补充系统在癌症中的矛盾作用.
- 为了突出最近关于细胞内补充功能的发现.
- 讨论了解补充在瘤学中的作用的挑战和未来方向.
主要方法:
- 评论最近的科学文献.
- 对基因表达数据的分析 (已知的局限性).
- 讨论新兴技术,如基因编辑和单细胞分析.
主要成果:
- 补充系统表现出瘤抑制和促进瘤的活动.
- 细胞内补充激活会影响瘤的扩散,免疫逃避和转移.
- 瘤利用补充剂来抑制免疫力和抵抗治疗.
- 细胞内补充系统 (complosome) 的概念表明在新陈代谢和应激反应中的作用.
结论:
- 补充剂在癌症中的作用是复杂的,超出了细胞外功能.
- 了解细胞内补充信号对于癌症研究至关重要.
- 需要使用先进技术进行进一步的研究,以开发针对补充系统的新型癌症疗法.
相关概念视频
Complement System
2.8K
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
2.8K
Metastasis
5.7K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.7K
The Tumor Microenvironment
6.8K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
6.8K
Adaptive Mechanisms in Cancer Cells
5.9K
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,...
5.9K
Cancer Cell Migration through Invadopodia
2.4K
Invadosome is a broad category of cell surface structures with proteolytic activity that degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
2.4K
The Intrinsic Apoptotic Pathway
6.9K
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...
6.9K


