Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Abnormal Proliferation

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...

Nucleotide Excision Repair

Nucleotide Excision Repair

You might also read

Related Articles

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

Sort by

Same author

Cdk1-phosphorylated Nur77 accumulates at the centrosome during mitosis to regulate the Cep192-PLK1 signaling axis.

Cell death & disease·2026

Same author

Disrupting the Formation of YAP Condensates Promotes the Activation of AMPKα to Inhibit the Progression of Primary Liver Cancer.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026

Same author

Cobalt- and ionic liquid-functionalized covalent organic framework for cooperative catalytic CO<sub>2</sub> cycloaddition.

Chemical communications (Cambridge, England)·2025

Same author

RXR<i>α</i> modulates hepatic stellate cell activation and liver fibrosis by targeting CaMKK<i>β</i>-AMPK<i>α</i> axis.

Acta pharmaceutica Sinica. B·2025

Same author

Halogenated retinoid derivatives as dual RARα and RXRα modulators for treating acute promyelocytic leukemia cells.

European journal of medicinal chemistry·2024

Same author

ErbB3 is required for hyperaminoacidemia-induced pancreatic α cell hyperplasia.

The Journal of biological chemistry·2024

Search research articles

Related Experiment Video

Updated: Jan 2, 2026

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

Targeting Nur77 translocation.

Xiao-kun Zhang¹

¹Burnham Institute for Medical Research, Cancer Center, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA. xzhang@burnham.org

Expert Opinion on Therapeutic Targets

|December 8, 2006

Summary

Nur77, a nuclear receptor, controls cancer cell survival and death. Inducing its migration to mitochondria triggers apoptosis, offering a new cancer treatment strategy targeting Nur77 translocation.

Area of Science:

Molecular Biology
Cancer Research
Cell Biology

Background:

Tumor growth is determined by cancer cell proliferation and death (apoptosis).
Nur77 (TR3/NGFI-B), an orphan nuclear receptor, regulates cancer cell survival and apoptosis.
Subcellular localization dictates Nur77's function: nuclear Nur77 promotes survival, while mitochondrial Nur77 induces apoptosis.

Purpose of the Study:

To investigate the role of Nur77 subcellular localization in cancer cell apoptosis.
To explore the potential of targeting Nur77 translocation for cancer therapy.

Main Methods:

Studied Nur77 localization and its impact on cancer cell apoptosis.
Investigated the effect of agents like AHPN/CD437 on Nur77 translocation.
Examined the role of retinoid X receptor (RXR) in regulating Nur77 translocation.

More Related Videos

Radionuclide-fluorescence Reporter Gene Imaging to Track Tumor Progression in Rodent Tumor Models

Radionuclide-fluorescence Reporter Gene Imaging to Track Tumor Progression in Rodent Tumor Models

Published on: March 13, 2018

Production of Nurr-1 Specific Polyclonal Antibodies Free of Cross-reactivity Against Its Close Homologs, Nor1 and Nur77

Production of Nurr-1 Specific Polyclonal Antibodies Free of Cross-reactivity Against Its Close Homologs, Nor1 and Nur77

Published on: August 17, 2015

Related Experiment Videos

Last Updated: Jan 2, 2026

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

Radionuclide-fluorescence Reporter Gene Imaging to Track Tumor Progression in Rodent Tumor Models

Radionuclide-fluorescence Reporter Gene Imaging to Track Tumor Progression in Rodent Tumor Models

Published on: March 13, 2018

Production of Nurr-1 Specific Polyclonal Antibodies Free of Cross-reactivity Against Its Close Homologs, Nor1 and Nur77

Production of Nurr-1 Specific Polyclonal Antibodies Free of Cross-reactivity Against Its Close Homologs, Nor1 and Nur77

Published on: August 17, 2015

Main Results:

Nur77's migration from the nucleus to mitochondria triggers apoptosis by binding Bcl-2 and causing cytochrome c release.
Agents like AHPN/CD437 effectively induce cancer cell apoptosis by promoting Nur77 translocation.
Retinoid X receptor (RXR) plays a crucial role in controlling Nur77 translocation.

Conclusions:

Nur77 translocation to mitochondria represents a novel mechanism for inducing cancer cell apoptosis.
Targeting Nur77 translocation with AHPN/CD437 or RXR ligands offers a promising therapeutic strategy to inhibit cancer growth by promoting cell death and reducing proliferation.