Related Experiment Video

Updated: Mar 4, 2026

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
04:20

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

1.5K

NDRG2 promotes adriamycin sensitivity through a Bad/p53 complex at the mitochondria in breast cancer

Yifang Wei1, Shentong Yu1,2, Yongping Zhang3

  • 1State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.

Oncotarget
|April 21, 2017
PubMed

Insights

N-Myc downstream-regulated gene 2 (NDRG2) enhances Adriamycin sensitivity in breast cancer by promoting apoptosis and cellular damage responses. This effect is p53-dependent, with NDRG2 preventing p53 nuclear entry to regulate chemo-resistance.

Area of Science:

  • Molecular Oncology
  • Cancer Therapeutics
  • Cellular Biology

Background:

  • Chemo-resistance is a significant obstacle in breast cancer treatment.
  • N-Myc downstream-regulated gene 2 (NDRG2) has been implicated in p53-mediated apoptosis during chemotherapy.
  • The precise mechanism of NDRG2's role in chemo-resistance remains largely unknown.

Purpose of the Study:

  • To investigate the role of NDRG2 in Adriamycin (ADR) resistance in breast cancer.
  • To elucidate the mechanism by which NDRG2 influences chemo-sensitivity.
  • To determine the involvement of p53 in NDRG2-mediated chemo-resistance.

Main Methods:

  • Analysis of NDRG2 expression in Adriamycin (ADR)-resistant breast cancer cells.
  • Assessment of NDRG2's impact on proliferation, cellular damage responses, and apoptosis.
  • Investigation of NDRG2's effect on p53 localization and Bad protein half-life.

Main Results:

  • NDRG2 expression was found to be decreased in ADR-resistant breast cancer cells.
  • Overexpression of NDRG2 enhanced ADR sensitivity by inhibiting proliferation and promoting apoptosis.
  • NDRG2 upregulates Bad expression by increasing its half-life, facilitating p53 mitochondrial association, and preventing p53 nuclear entry.

Conclusions:

  • NDRG2 plays a crucial role in enhancing breast cancer sensitivity to Adriamycin.
  • The chemo-sensitizing effect of NDRG2 is dependent on p53, specifically by inhibiting p53 nuclear translocation.
  • NDRG2 influences chemo-resistance not by altering p53 expression levels but by modulating its cellular localization and downstream effects.
Keywords:
BadNDRG2P53breast cancerchemotherapy resistance

More Related Videos

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method09:32

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method

Published on: September 10, 2017

11.5K
Establishing Cell Lines Overexpressing DR3 to Assess the Apoptotic Response to Anti-mitotic Therapeutics12:28

Establishing Cell Lines Overexpressing DR3 to Assess the Apoptotic Response to Anti-mitotic Therapeutics

Published on: January 11, 2019

7.8K

Related Concept Videos

Abnormal Proliferation02:23

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...
5.3K
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
38.7K
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
56
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
19.3K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
10.3K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
3.3K