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 Experiment Videos

Cellular transformation and malignancy induced by ras require c-jun

R Johnson1, B Spiegelman, D Hanahan

  • 1Hormone Research Institute, University of California, San Francisco 94143, USA.

Molecular and Cellular Biology
|August 1, 1996
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Increased invasiveness of MMP-9-deficient tumors in two mouse models of neuroendocrine tumorigenesis.

Oncogene·2012
Same author

Combining antiangiogenic agents with metronomic chemotherapy enhances efficacy against late-stage pancreatic islet carcinomas in mice.

Cold Spring Harbor symposia on quantitative biology·2003
Same author

Genome scanning with array CGH delineates regional alterations in mouse islet carcinomas.

Nature genetics·2001
Same author

CREB regulates hepatic gluconeogenesis through the coactivator PGC-1.

Nature·2001
Same author

L-selectin can facilitate metastasis to lymph nodes in a transgenic mouse model of carcinogenesis.

Proceedings of the National Academy of Sciences of the United States of America·2001
Same author

Cell factories for fighting cancer.

Nature biotechnology·2001
Same journal

Aberrant Expression of miR-25-3p/EZH2 Is Involved in T Cell Activation in Aplastic Anemia.

Molecular and cellular biology·2026
Same journal

Characterization of the m<sup>6</sup>A Epitranscriptome in Fibroblast Senescence.

Molecular and cellular biology·2026
Same journal

Insights into FACT in Cancers with Targeted Therapeutic Implications.

Molecular and cellular biology·2026
Same journal

Human lncRNA, hLinfRNA7 (IDO1-AS) Regulates Cytokine Expression, Tryptophan Catabolism, and Inflammatory Response in Macrophage.

Molecular and cellular biology·2026
Same journal

mTORC1-Dependent Regulation of the CCL24-CCR3 Axis Controls Granuloma Formation and Maintenance in Sarcoidosis.

Molecular and cellular biology·2026
Same journal

The Novel Compound SIC-19 Triggers CUL4B-Mediated Ubiquitination and Degradation of SIK2.

Molecular and cellular biology·2026
See all related articles

Ras oncogene activation relies on the transcription factor AP-1, specifically c-Jun. Loss of c-Jun impairs Ras-driven cell transformation, but restoring c-Jun rescues these properties, confirming its critical role.

Area of Science:

  • Oncogenes and cancer biology
  • Molecular mechanisms of cell transformation
  • Transcription factor regulation

Background:

  • Ras is a key oncogene implicated in various cancers.
  • Activated Ras proteins induce the AP-1 transcription factor, a complex of Fos and Jun proteins.
  • Dysregulated AP-1 protein expression can lead to neoplastic transformation, suggesting AP-1 as a Ras effector.

Purpose of the Study:

  • To investigate the role of AP-1 as a critical effector of Ras-induced transformation.
  • To determine if c-Jun is essential for Ras-mediated cellular changes and tumorigenicity.

Main Methods:

  • Analysis of Ras-induced transcriptional responses in c-jun null fibroblasts.
  • Comparison of transformation characteristics (loss of contact inhibition, anchorage independence, tumorigenicity) between wild-type and c-jun null cells.

Related Experiment Videos

  • Restoration of c-Jun expression in c-jun null cells to assess rescue of transformation phenotypes.

    • Main Results:

    • Ras-induced transcriptional activation of AP-1-responsive genes was significantly impaired in c-jun null fibroblasts.
    • c-jun null cells exhibited a lack of key Ras transformation hallmarks compared to wild-type cells.
    • Forced expression of c-Jun restored contact inhibition, anchorage independence, and tumorigenicity in Ras-expressing c-jun null cells.
    • Tumorigenic variants arising from Ras-expressing c-jun null cells consistently showed restored AP-1 activity.

    Conclusions:

    • c-Jun is a crucial effector for transformation induced by activated Ras proteins.
    • Genetic evidence supports c-Jun's essential role in mediating Ras-driven oncogenesis.
    • Targeting the Ras-c-Jun pathway may offer therapeutic strategies for Ras-driven cancers.