Jove
Visualize
联系我们
JoVE
x logofacebook logolinkedin logoyoutube logo
关于 JoVE
概览领导团队博客JoVE 帮助中心
作者
出版流程编辑委员会范围与政策同行评审常见问题投稿
图书馆员
用户评价订阅访问资源图书馆顾问委员会常见问题
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experiments存档
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教师资源中心教师网站
使用条款与条件
隐私政策
政策

相关概念视频

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

7.9K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.9K
Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

2.3K
Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012...
2.3K
Methods of Nuclear Reprogramming01:24

Methods of Nuclear Reprogramming

1.9K
Nuclear reprogramming is a process of transforming one cell type into an unrelated cell type by epigenetic changes that alter the cell’s original gene expression pattern. Such epigenetic changes force cells to express a different set of genes, which play a significant role in inducing transformation into other cell types. Nuclear reprogramming offers applications in reproductive cloning for livestock propagation and regenerative medicine — developing patient-specific cells for...
1.9K
Stem Cell Niche01:26

Stem Cell Niche

5.3K
The stem cell niche is the dynamic microenvironment where stem cells reside. Inside these niches, the cells may remain undifferentiated, undergo high self-renewal, or become lineage-specific progenitors. Stem cells coexist with other niche cells, such as stromal cells. They also interact closely with the ECM. Cell-cell and cell-matrix communication occur via adhesion molecules or soluble factors that signal the stem cells and determine their fate. Stromal cells also provide survival signals to...
5.3K
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

5.1K
Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
5.1K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

6.6K
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
6.6K

您也可能阅读

相关文章

通过共同作者、期刊和引用图与本文相关的文章。

排序
Same author

Single cell multiomics unravel the transcription networks controlling the different EMT tumor states.

Nature communications·2026
Same author

A stretch-responsive fibroblast program promotes epidermal stem cell self-renewal during skin expansion.

Nature communications·2026
Same author

Cell stiffness regulates immune evasion during metastatic dormancy.

Nature cancer·2026
Same author

Multi-omics integration and batch correction using a modality-agnostic deep learning framework.

bioRxiv : the preprint server for biology·2025
Same author

Author Correction: Mechanisms of stretch-mediated skin expansion at single-cell resolution.

Nature·2025
Same author

Identification, functional insights and therapeutic targeting of EMT tumour states.

Nature reviews. Cancer·2025

相关实验视频

Updated: Sep 18, 2025

Evaluating the Differentiation Capacity of Mouse Prostate Epithelial Cells Using Organoid Culture
10:38

Evaluating the Differentiation Capacity of Mouse Prostate Epithelial Cells Using Organoid Culture

Published on: November 22, 2019

9.1K

天生的免疫和NF-κB通路控制前列腺干细胞的可塑性,重编程和瘤启动.

Chen Jiang1, Yura Song1, Sandrine Rorive2

  • 1Laboratory of Stem Cells and Cancer, Université Libre de Bruxelles (ULB), Brussels, Belgium.

Nature cancer
|June 23, 2025
PubMed
概括

在前列腺基细胞 (BCs) 中删除Pten会触发细胞可塑性和瘤启动. 针对IL-1,JAK-STAT和NF-κB等先天免疫路径,可以抑制这种Pten诱导的重编程,从而提供新的前列腺癌治疗策略.

更多相关视频

In vitro Enrichment of Ovarian Cancer Tumor-initiating Cells
11:37

In vitro Enrichment of Ovarian Cancer Tumor-initiating Cells

Published on: February 18, 2015

13.9K
Isolation of Stem-like Cells from 3-Dimensional Spheroid Cultures
09:06

Isolation of Stem-like Cells from 3-Dimensional Spheroid Cultures

Published on: December 13, 2019

9.3K

相关实验视频

Last Updated: Sep 18, 2025

Evaluating the Differentiation Capacity of Mouse Prostate Epithelial Cells Using Organoid Culture
10:38

Evaluating the Differentiation Capacity of Mouse Prostate Epithelial Cells Using Organoid Culture

Published on: November 22, 2019

9.1K
In vitro Enrichment of Ovarian Cancer Tumor-initiating Cells
11:37

In vitro Enrichment of Ovarian Cancer Tumor-initiating Cells

Published on: February 18, 2015

13.9K
Isolation of Stem-like Cells from 3-Dimensional Spheroid Cultures
09:06

Isolation of Stem-like Cells from 3-Dimensional Spheroid Cultures

Published on: December 13, 2019

9.3K

科学领域:

  • 前列腺癌研究前列腺癌研究.
  • 干细胞生物学 干细胞生物学
  • 癌症表观遗传学 癌症表观遗传学

背景情况:

  • 前列腺上皮来自于多能干细胞,在成年人中分化为受血统限制的基底细胞和光细胞.
  • 基底细胞 (BCs) 中的Pten损失可以恢复多能性,但BC可塑性和瘤启动的机制仍然不清楚.

研究的目的:

  • 为了研究基底细胞可塑性和前列腺瘤启动后的Pten删除背后的分子机制.
  • 根据Pten驱动的重编程来确定前列腺癌的潜在治疗点.

主要方法:

  • 单细胞RNA测序和ATAC-seq被用来分析Pten删除后的细胞命运变化.
  • 实地表征和关键信号通路的药理/遗传抑制进行了.

主要成果:

  • 前列腺BCs中的Pten删除诱导了区域化的细胞命运重编程,其特征是通过山丘状和近端状光状态的进展.
  • 这种重编程与先天性免疫信号通路的激活有关,包括互白素-1,JAK-STAT和NF-κB.
  • 这些途径的抑制,无论是药理上还是遗传上,都有效地阻止了Pten诱导的BC可塑性和重编程.

结论:

  • 通过定义的细胞命运轨迹,Pten损失驱动前列腺基底细胞可塑性和瘤启动.
  • 天生的免疫路径是Pten驱动的前列腺癌发展的关键调解者.
  • 准IL-1,JAK-STAT和NF-κB通路为前列腺癌的预防和治疗提供了一个有前途的战略.