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

Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

5.0K
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...
5.0K
The Tumor Microenvironment02:17

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
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

5.1K
Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
5.1K
Cancer Cell Migration through Invadopodia01:35

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
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

3.4K
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.4K
Metastasis02:30

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...
5.7K

You might also read

Related Articles

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

Sort by
Same author

Integrating Extracellular Matrix Dynamics and Membrane-Associated Signaling: The Role of Clusterin-LRP1 Network in Cancer Cell Migration and Tumor Progression.

Cancers·2026
Same author

Integrative Survival Prediction in Breast Cancer Using Extracellular Matrix Protease Transcript Signatures and Clinical Variables: A Machine Learning Approach.

Cancers·2026
Same author

Effects of Acidic Polysaccharide-Enriched Extracts from <i>Holothuria tubulosa</i> on Two- and Three-Dimensional Invasive Breast Cancer Cell Models.

Biology·2025
Same author

Isolated prolapse of the posterior mitral valve leaflet: phenotypic refinement, heritability and genetic etiology.

medRxiv : the preprint server for health sciences·2024
Same author

Growth and Physiological Characteristics of Strawberry Plants Cultivated under Greenhouse-Integrated Semi-Transparent Photovoltaics.

Plants (Basel, Switzerland)·2024
Same author

Redefining metalloproteases specificity through network proteolysis.

Trends in molecular medicine·2023

Related Experiment Video

Updated: Aug 31, 2025

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
06:35

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth

Published on: December 22, 2020

4.6K

Interplay Between Chemotherapy-Activated Cancer Associated Fibroblasts and Cancer Initiating Cells Expressing CD44v6

Shibnath Ghatak1,2, Vincent C Hascall3, Nikos Karamanos4

  • 1Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC, United States.

Frontiers in Oncology
|August 19, 2022
PubMed
Summary

Chemotherapy resistance in colorectal cancer is driven by cancer-initiating cells (CICs) interacting with cancer-associated fibroblasts. Targeting CD44v6 expression on CICs can overcome this resistance and reduce tumor growth.

Keywords:
CD44v6CD44v6-therapyIL17AWNT3Acancer associate fibroblasts (CAFs)cancer initiating cells (CICs)colorectal cancer (CRC)periostin

More Related Videos

Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies
09:01

Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies

Published on: July 3, 2025

230
A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication
09:52

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication

Published on: September 20, 2016

10.4K

Related Experiment Videos

Last Updated: Aug 31, 2025

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
06:35

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth

Published on: December 22, 2020

4.6K
Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies
09:01

Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies

Published on: July 3, 2025

230
A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication
09:52

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication

Published on: September 20, 2016

10.4K

Area of Science:

  • Oncology
  • Cancer Biology
  • Nanomedicine

Background:

  • Cancer-initiating cells (CICs) are crucial drivers of colorectal tumor growth and persistence.
  • The tumor microenvironment, particularly cancer-associated fibroblasts (CAFs), plays a significant role in supporting CICs.
  • Chemotherapeutic agents like FOLFOX can paradoxically enhance tumor-promoting properties of CICs and their microenvironment.

Purpose of the Study:

  • To investigate the interplay between colorectal CICs and CAFs in response to FOLFOX chemotherapy.
  • To elucidate the mechanisms by which CAFs promote chemotherapy resistance in CICs.
  • To develop and evaluate novel therapeutic strategies targeting this interaction for colorectal cancer treatment.

Main Methods:

  • Analysis of CD44v6 expression in CICs and its correlation with FOLFOX resistance.
  • Identification of CAF-secreted factors (periostin, IL17A, WNT3A) that enhance CIC immunophenotype.
  • Development of nanoparticle-encapsulated vectors for tissue-specific conditional silencing of CD44v6 in vivo.

Main Results:

  • FOLFOX treatment enhances CD44v6 expression on CICs, mediated by CAF-secreted factors activating WNT3A/β-catenin signaling.
  • Tissue-specific silencing of CD44v6 using novel nanoparticle vectors significantly reduced colorectal tumor growth.
  • This silencing demonstrated long-lasting effects on tumor self-renewal and growth, linked to a WNT3A/CD44 feedback loop.

Conclusions:

  • Therapeutic strategies must consider the interplay between stromal factors and CIC immunophenotype for effective cancer treatment.
  • Targeting the chemotherapy-induced enrichment of CD44v6 positive CICs represents a promising therapeutic approach.
  • Nanoparticle-mediated gene silencing offers a potent method to block pro-tumorigenic paracrine signaling in colorectal cancer.