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

Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

3.5K
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...
3.5K
Mitogens and the Cell Cycle02:38

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
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

5.6K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.6K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

3.8K
3.8K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.6K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.6K
Cell Migration01:19

Cell Migration

6.0K
Cell migration is a process by which the cells move from one location to another, playing an essential role in embryological development, repair and regeneration, immune response, and metastasis. Cells migrate in response to chemical or mechanical signals generated by specific organs or tissues. The overall mechanism includes three steps - polarization, protrusion, and release. Polarization involves the formation of a distinct cell front and rear, which determines the direction of movement.
6.0K

You might also read

Related Articles

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

Sort by
Same author

Astrocytic connexin43 phosphorylation contributes to seizure susceptibility after mild traumatic brain injury.

The FEBS journal·2026
Same author

Proteomic and Metabolomic Analysis of PCK2-Dependent Alterations in Group 3 Medulloblastoma Cells.

Journal of proteome research·2026
Same author

Long-term Survival and Molecular Biomarker Evaluation of a Phase II Cetuximab and Nivolumab Clinical Trial in Recurrent/Metastatic Head and Neck Cancer.

Clinical cancer research : an official journal of the American Association for Cancer Research·2025
Same author

Immunoinformatics-Based Multi-Epitope Vaccine Design Against <i>P. falciparum-</i>Causing Malaria: A Computational Approach.

Health science reports·2025
Same author

Targeting S100A9-mediated inflammation: a novel therapeutic approach for CLL.

Blood advances·2025
Same author

CRISPR-Drug Combinatorial Screening Identifies Effective Combination Treatments for MTAP-Deleted Cancer.

Cancer research·2025

Related Experiment Video

Updated: Apr 25, 2026

Studying TGF-&#946; Signaling and TGF-&#946;-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

13.0K

Adaptive Responses Directed by CREB Control Epithelial-Mesenchymal Plasticity in Cancer.

Kshitij Parag-Sharma, Harish Bharambe, John J Powers

    Biorxiv : the Preprint Server for Biology
    |April 24, 2026
    PubMed
    Summary
    This summary is machine-generated.

    Cellular plasticity, crucial for development, involves epithelial-mesenchymal transition (EMT) intermediates. The transcription factor CREB controls these hybrid states in cancer, coordinating VGLL3 and KLF3 to drive metastasis.

    More Related Videos

    Induction and Analysis of Epithelial to Mesenchymal Transition
    10:37

    Induction and Analysis of Epithelial to Mesenchymal Transition

    Published on: August 27, 2013

    38.0K
    Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
    11:42

    Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

    Published on: April 7, 2017

    8.4K

    Related Experiment Videos

    Last Updated: Apr 25, 2026

    Studying TGF-&#946; Signaling and TGF-&#946;-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
    06:54

    Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

    Published on: October 27, 2020

    13.0K
    Induction and Analysis of Epithelial to Mesenchymal Transition
    10:37

    Induction and Analysis of Epithelial to Mesenchymal Transition

    Published on: August 27, 2013

    38.0K
    Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
    11:42

    Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

    Published on: April 7, 2017

    8.4K

    Area of Science:

    • Cellular plasticity and cancer biology
    • Molecular mechanisms of metastasis
    • Transcriptional regulation in cancer

    Background:

    • Cellular plasticity, including epithelial-mesenchymal transition (EMT), is vital for development and tissue homeostasis.
    • EMT is a dynamic continuum of metastable states, not a binary switch, with hybrid epithelial-mesenchymal (E/M) states promoting cancer progression.
    • Understanding the regulation of these hybrid E/M states is critical for targeting cancer metastasis, drug resistance, and recurrence.

    Purpose of the Study:

    • To elucidate the molecular mechanisms controlling metastable hybrid E/M states in cancer.
    • To identify key regulators of E/M plasticity that promote cancer cell adaptation and metastasis.
    • To validate the role of the transcription factor CREB in regulating cancer cell plasticity and metastasis.

    Main Methods:

    • Utilized a CREB-dependent head and neck cancer model to study E/M plasticity.
    • Analyzed a non-canonical EMT gene signature regulated by CREB across various cancer types.
    • Performed gain- and loss-of-function studies to establish the roles of CREB, VGLL3, and KLF3 in E/M plasticity and metastasis.

    Main Results:

    • Demonstrated that the master transcription factor CREB controls adaptive response genes essential for E/M plasticity.
    • Identified a CREB-dependent, non-canonical EMT gene signature crucial for hybrid E/M states.
    • Revealed VGLL3 and KLF3 as core PanCancer mediators of hybrid E/M states, regulated by CREB.
    • Established that CREB coordinates VGLL3 and KLF3 to drive cancer cell metastasis.

    Conclusions:

    • CREB is a master regulator of cancer cell plasticity, controlling hybrid E/M states.
    • CREB coordinates the transcriptional regulators VGLL3 and KLF3 to drive metastasis.
    • Targeting the CREB-VGLL3-KLF3 axis offers a potential strategy for inhibiting cancer progression and metastasis.