相关实验视频
Updated: Jul 3, 2025

10:37
Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
35.8K
在宫癌中,Atractylodes macrocephala III通过通过ETV5调节IGF2BP3,从而抑制EMT
Meixia Wang1,2, Jingwen Meng3, Hongyun Wang4
1Department of Gynecology and Obstetrics, Nanjing Drum Tower Hospital, Clinical College of Nanjing University of Chinese Medicine, Nanjing, China.
Journal of cellular and molecular medicine
|February 15, 2024
概括
甲状腺巨头III (ATLIII) 通过ETV5通路抑制胰岛素样生长因子2和mRNA结合蛋白3 (IGF2BP3) 的下调,从而抑制宫癌细胞的迁移和入侵.
科学领域:
- 在瘤学瘤学.
- 药理学 药理学是指药理学的学科.
- 分子生物学分子生物学
背景情况:
- 亚特拉提洛德斯巨头三号 (ATL三号) 具有抗炎和抗瘤的特性.
- 关于ATL III对子宫癌的具体影响和机制在很大程度上是未知的.
- 胰岛素样生长因子2 mRNA结合蛋白3 (IGF2BP3) 在宫癌组织中表达高.
研究的目的:
- 研究ATL III对子宫癌细胞的影响.
- 阐明ATL III对宫癌的作用背后的分子机制.
- 确定宫癌治疗的潜在治疗点.
主要方法:
- RNA测序 (RNA-Seq) 用于识别差异表达的基因.
- 使用HeLa和SiHa宫癌细胞系进行细胞培养实验.
- 通过小干扰RNA (siRNA) 和过度表达等离子体进行传染,以操纵IGF2BP3水平.
- 使用JASPAR系统进行生物信息分析来预测转录因子.
主要成果:
- 在ATL III下调节宫癌细胞中IGF2BP3的表达.
- 在宫癌细胞中,ATL III促进了亡并调节了上皮-介质细胞过渡 (EMT).
- IGF2BP3表达水平与宫癌细胞迁移和入侵相关.
- ATL III 抑制ETV5,一种促进IGF2BP3表达的转录因子.
- 过度表达IGF2BP3减弱了ATL III对细胞迁移和侵入的抑制作用.
结论:
- ATL III 抑制了宫癌细胞的迁移和入侵.
- 该机制涉及IGF2BP3的下调,IGF2BP3是细胞运动的关键调节者.
- ATL III通过抑制ETV5-IGF2BP3通路来发挥其作用.
- ATL III显示出作为治疗宫癌的治疗剂的潜力.
相关概念视频
Cadherins in Tissue Organization
3.0K
The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
Cell Sorting During Development
Cell sorting plays an...
Cell Sorting During Development
Cell sorting plays an...
3.0K
Metastasis
5.5K
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...
5.5K
Mitogens and the Cell Cycle
6.5K
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...
6.5K
Cancer Cell Migration through Invadopodia
2.3K
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,...
2.3K
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
Role Of Notch Signalling In Intestinal Stem Cell Renewal
2.1K
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.1K

