Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

3.0K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
3.0K
Abnormal Proliferation02:23

Abnormal Proliferation

4.4K
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...
4.4K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

4.7K
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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
4.7K
Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

11.4K
As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
11.4K
Negative Regulator Molecules01:23

Negative Regulator Molecules

35.1K
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.
35.1K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

4.6K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.6K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Lung carcinoids with sustentacular cells and low keratin expression: A common yet under-recognized phenomenon with diagnostic and biological implications.

Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc·2026
Same author

Retraction Note: NSD2 targeting reverses plasticity and drug resistance in prostate cancer.

Nature·2026
Same author

HMGCS1 drives cholesterol-dependent membrane repair and shields tumor cells from lymphocyte attack.

Nature communications·2026
Same author

Dependencies in heterogeneous, lineage plastic patient-derived prostate cancer organoids revealed through integrated single-cell multiomics and CRISPR screening.

bioRxiv : the preprint server for biology·2026
Same author

Compression-induced metabolic adaptation drives confined tumor cell migration and distant metastasis via malate-dependent microtubule reinforcement.

Cell research·2026
Same author

CD300ld on pathologically activated neutrophils promotes tumor immune suppression by binding phosphatidylserine on CD8<sup>+</sup> T cells.

Nature cancer·2026

Related Experiment Video

Updated: Jun 4, 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

8.8K

LKB1 inactivation promotes epigenetic remodeling-induced lineage plasticity and antiandrogen resistance in prostate

Fei Li1, Pengfei Dai1,2, Huili Shi1,2

  • 1Key Laboratory of Multi-Cell Systems, Shanghai Key Laboratory of Molecular Andrology, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, China.

Cell Research
|January 1, 2025
PubMed
Summary

Liver kinase B1 (LKB1) pathway inactivation drives androgen receptor (AR)-independent lineage plasticity in castration-resistant prostate cancer (CRPC). Targeting DNA hypomethylation offers a novel therapeutic strategy for CRPC.

More Related Videos

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

17.8K
Murine Prostate Micro-dissection and Surgical Castration
08:49

Murine Prostate Micro-dissection and Surgical Castration

Published on: May 11, 2016

45.4K

Related Experiment Videos

Last Updated: Jun 4, 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

8.8K
Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

17.8K
Murine Prostate Micro-dissection and Surgical Castration
08:49

Murine Prostate Micro-dissection and Surgical Castration

Published on: May 11, 2016

45.4K

Area of Science:

  • Cancer biology and epigenetics
  • Prostate cancer research
  • Molecular mechanisms of tumor progression

Background:

  • Epigenetic regulation influences cancer cell fate, heterogeneity, and therapy response.
  • Androgen receptor (AR)-independent lineage plasticity in castration-resistant prostate cancer (CRPC) is poorly understood, limiting effective treatments.
  • Understanding the molecular drivers of CRPC progression is crucial for developing new therapies.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying AR-independent lineage plasticity in CRPC.
  • To identify potential therapeutic strategies targeting AR-independent CRPC.
  • To elucidate the role of epigenetic alterations in CRPC progression.

Main Methods:

  • Single-cell RNA sequencing of human and mouse prostate cancer samples.
  • Whole-genome bisulfite sequencing.
  • Genetically engineered mouse models.
  • Pharmacological inhibition of TET enzymes and S-adenosyl methionine supplementation.

Main Results:

  • LKB1 pathway inactivation is associated with AR independence in human prostate cancer.
  • LKB1 inactivation promotes AR-independent lineage plasticity and global DNA hypomethylation.
  • Inhibition of TET enzymes and S-adenosyl methionine supplementation suppressed AR-independent CRPC growth.

Conclusions:

  • LKB1 inactivation is a key driver of AR-independent lineage plasticity in CRPC.
  • Global DNA hypomethylation is a critical epigenetic event in AR-independent CRPC progression.
  • Targeting DNA hypomethylation pathways presents a promising therapeutic strategy for AR-independent CRPC.