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

Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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...

You might also read

Related Articles

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

Sort by
Same author

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

Nature·2026
Same author

A forward genetic screen identifies Sirtuin1 as a driver of neuroendocrine prostate cancer.

The Journal of experimental medicine·2026
Same author

Cardiac conduction system malformations in heterotaxy result from dysregulated Pitx2 expression.

JCI insight·2026
Same author

Determinants of sensitivity to HER2-targeted antibody drug conjugates in urothelial cancer.

Nature communications·2025
Same author

NSD2 targeting reverses plasticity and drug resistance in prostate cancer.

Nature·2025
Same author

Combination regimen of intravesical docetaxel, gemcitabine, and cisplatin in patients with BCG-unresponsive bladder cancer: clinical outcomes and genomic correlations.

Urologic oncology·2025

Related Experiment Video

Updated: Jun 23, 2026

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
12:13

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients

Published on: November 19, 2019

Decrypting the role of Cripto in tumorigenesis.

Michael M Shen1

  • 1Center for Advanced Biotechnology and Medicine, 679 Hoes Lane, Piscataway, New Jersey 08854, USA. mshen@cabm.rutgers.edu

The Journal of Clinical Investigation
|August 20, 2003
PubMed
Summary

Cripto protein overexpression in epithelial cancers can promote tumor growth by blocking Activin B

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Cripto, a cell-surface protein, is frequently overexpressed in various epithelial cancers.
  • The precise mechanisms by which Cripto contributes to tumorigenesis remain largely unelucidated.
  • Understanding Cripto's role is crucial for developing targeted cancer therapies.

Discussion:

  • This study investigates the interaction between Cripto and the TGF-beta ligand Activin B.
  • Cripto binding to Activin B inhibits Activin B's tumor-suppressive functions.
  • This interaction disrupts normal cell proliferation control in cancerous tissues.

Key Insights:

  • Cripto directly interferes with Activin B signaling pathways.
  • Blocking Cripto's function can impede tumor progression.

More Related Videos

Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

Establishment of a Co-culture System of Patient-Derived Colorectal Tumor Organoids and Tumor-Infiltrating Lymphocytes (TILs)
08:42

Establishment of a Co-culture System of Patient-Derived Colorectal Tumor Organoids and Tumor-Infiltrating Lymphocytes (TILs)

Published on: June 27, 2025

Related Experiment Videos

Last Updated: Jun 23, 2026

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
12:13

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients

Published on: November 19, 2019

Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

Establishment of a Co-culture System of Patient-Derived Colorectal Tumor Organoids and Tumor-Infiltrating Lymphocytes (TILs)
08:42

Establishment of a Co-culture System of Patient-Derived Colorectal Tumor Organoids and Tumor-Infiltrating Lymphocytes (TILs)

Published on: June 27, 2025

  • The Cripto-Activin B axis represents a novel target for cancer treatment.

    • Outlook:

    • Antibody-based blockade of Cripto shows therapeutic potential for inhibiting tumorigenesis.
    • Further research into Cripto-targeted therapies may lead to new cancer treatments.
    • Investigating Cripto's broader role in cancer signaling pathways is warranted.