相关实验视频
Updated: May 12, 2025

08:42
Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
Published on: July 3, 2020
4.3K
编程死亡链接1调节了乳腺母细胞瘤的生长和复发
Linzhou Zhang1, Hao Lin1, Jiajie Liang1
1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
International journal of oral science
|April 16, 2025
概括
编程死亡配体1 (PD-L1) 通过增强细胞更新和入侵来推动乳腺母细胞瘤的生长和复发. 抑制PD-L1通路为这种瘤提供了潜在的治疗策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 编程死亡连接体1 (PD-L1) 内在信号驱动瘤进展,但其在乳腺母细胞瘤 (AM) 中的作用仍然未被探索.
- 骨髓母细胞瘤是一种局部侵袭性牙瘤,复发率高.
研究的目的:
- 研究PD-L1在乳腺母细胞瘤发病,进展和复发中的作用.
- 阐明潜在的分子机制,并评估PD-L1通路的治疗向.
主要方法:
- 在AM组织中分析PD-L1表达.
- 使用具有PD-L1过度表达或剥离的hTERT+-AM细胞的功能研究.
- 在AM患者中单细胞分析和免疫组织化学分析.
- 评估PD-L1-PI3K-AKT-mTOR信号轴的激活情况.
- 在患者衍生瘤器官中评估PD-L1阻塞.
主要成果:
- 在AM组织中,PD-L1被上调,与增加的瘤生长和复发相关.
- 过度表达PD-L1增强了AM细胞的自我更新,瘤性和入侵性.
- PD-L1激活PI3K-AKT-mTOR通路,促进部分上皮质-介质酶过渡.
- 针对PD-L1-PI3K-AKT-mTOR轴抑制了AM瘤有机体的生长.
结论:
- 瘤细胞内在的PD-L1信号传递是乳腺母细胞瘤攻击性和复发的关键驱动因素.
- PD-L1-PI3K-AKT-mTOR轴代表了乳腺母细胞瘤的一个关键的调节机制.
- 阻断PD-L1是一种有前途的治疗策略,用于乳腺母细胞瘤.
相关概念视频
Abnormal Proliferation
4.3K
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...
4.3K
Mitogens and the Cell Cycle
6.3K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.3K
The Intrinsic Apoptotic Pathway
5.6K
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...
5.6K
The Retinoblastoma Gene
4.0K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.0K
Regulation of Angiogenesis and Blood Supply
2.5K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.5K

