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

Function and dysfunction of the human oncoprotein MDM2.

Swati Palit Deb1

  • 1Department of Biochemistry and Molecular Biophysics and the Massey Cancer Center, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298, USA. Spdeb@hsc.vcu.edu

Frontiers in Bioscience : a Journal and Virtual Library
|January 10, 2002
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

Oncogenic p53 induces mitotic errors in lung cancer cells by recopying DNA replication forks conferring targetable proliferation advantage.

Cell death and differentiation·2026
Same author

Oncogenic p53 induces mitotic errors in lung cancer cells by recopying DNA replication forks conferring targetable proliferation advantage.

Research square·2025
Same author

Oncogenic Mutant p53 Sensitizes Non-Small Cell Lung Cancer Cells to Proteasome Inhibition via Oxidative Stress-Dependent Induction of Mitochondrial Apoptosis.

Cancer research communications·2024
Same author

Inhalant cannabidiol impedes tumor growth through decreased tumor stemness and impaired angiogenic switch in NCI-H1437-induced human lung cancer model.

Human cell·2023
Same author

The oncogenicity of tumor-derived mutant p53 is enhanced by the recruitment of PLK3.

Nature communications·2021
Same author

DNA replication in progenitor cells and epithelial regeneration after lung injury requires the oncoprotein MDM2.

JCI insight·2019
Same journal

The CD44 protein family: roles in embryogenesis and tumor progression.

Frontiers in bioscience : a journal and virtual library·2017
Same journal

Four varieties of voltage-gated proton channels.

Frontiers in bioscience : a journal and virtual library·2017
Same journal

Lurie's tubercle-count method to test TB vaccine efficacy in rabbits.

Frontiers in bioscience : a journal and virtual library·2017
Same journal

Optical spectroscopy of breast biopsies and human breast cancer xenografts in nude mice.

Frontiers in bioscience : a journal and virtual library·2017
Same journal

The colostrum-deprived, artificially-reared, neonatal pig as a model animal for studying rotavirus gastroenteritis.

Frontiers in bioscience : a journal and virtual library·2017
Same journal

Action of polypeptide growth factors in colon cancer; development of new therapeutic approaches.

Frontiers in bioscience : a journal and virtual library·2017
See all related articles

The double minute-2 (MDM2) oncoprotein promotes cancer by inactivating tumor suppressor p53 and regulating cell cycle progression. Understanding MDM2

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The double minute-2 (mdm2) gene product, MDM2, is frequently overexpressed in human cancers.
  • MDM2 possesses oncogenic properties, partly due to its ability to inactivate the tumor suppressor p53.
  • MDM2 interacts with cell cycle regulators, contributing to its tumorigenic potential.

Purpose of the Study:

  • To investigate the oncogenic functions of MDM2.
  • To understand the role of MDM2 in cell cycle regulation and tumorigenesis.
  • To explore the implications of MDM2's growth regulatory functions for cancer drug development.

Main Methods:

  • Analysis of MDM2 overexpression in tumors.
  • Investigation of MDM2 gene amplification effects on cell transformation.

Related Experiment Videos

  • Studies on MDM2's interaction with p53 and cell cycle proteins.
  • Examination of MDM2-mediated cell cycle arrest (G1 to S phase transition).

    • Main Results:

    • MDM2 overexpression and gene amplification enhance tumorigenic potential.
    • MDM2 inactivates p53 and interacts with cell cycle proteins.
    • Full-length MDM2 overexpression arrests cells at G1/S phase; domain elimination induces tumorigenesis.
    • Some cancer cells exhibit insensitivity to MDM2-induced growth arrest.

    Conclusions:

    • MDM2 plays a significant role in cancer development through p53 inactivation and cell cycle dysregulation.
    • Defects in MDM2-mediated growth arrest or cellular insensitivity contribute to tumorigenesis.
    • Further elucidation of MDM2's growth regulatory functions could lead to novel cancer therapeutics.