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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
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...
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...

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Related Experiment Video

Updated: Jul 13, 2026

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

Targeting c-Jun and JunB proteins as potential anticancer cell therapy.

E N Gurzov1, L Bakiri, J M Alfaro

  • 1Department of Molecular Biology, Facultad de Ciencias, Centro de Biología Molecular Severo Ochoa, Universidad Autónoma de Madrid, Cantoblanco, Madrid, Spain.

Oncogene
|August 2, 2007
PubMed
Summary

Jun proteins regulate cell proliferation and tumor growth. Inhibiting both JunB and c-Jun shows promise as an antitumor strategy by inducing cancer cell death and extending survival.

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A Flow Cytometry-Based Cell Surface Protein Binding Assay for Assessing Selectivity and Specificity of an Anticancer Aptamer
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Last Updated: Jul 13, 2026

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

A Flow Cytometry-Based Cell Surface Protein Binding Assay for Assessing Selectivity and Specificity of an Anticancer Aptamer
10:46

A Flow Cytometry-Based Cell Surface Protein Binding Assay for Assessing Selectivity and Specificity of an Anticancer Aptamer

Published on: September 13, 2022

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Activating protein-1 (AP-1) transcription factors, especially Jun proteins, are crucial in cell proliferation and tumor development.
  • Understanding the role of JunB in tumor progression is vital for developing new cancer therapies.

Purpose of the Study:

  • To investigate the clinical relevance of targeting JunB expression in cancer.
  • To explore the combined effects of JunB knockdown and c-Jun/JNK pathway inhibition on tumor growth and survival.

Main Methods:

  • Utilized retroviruses to generate short hairpin RNA (shRNA) for reducing JunB levels.
  • Examined the impact of JunB reduction on proliferation and tumorigenicity in wild-type and c-Jun knockout murine fibroblasts.
  • Investigated the effects of combined JunB knockdown and c-Jun/JNK inactivation in melanoma-derived B16-F10 cancer cells and in vivo mouse models.

Main Results:

  • JunB reduction increased proliferation and tumorigenicity in wild-type cells.
  • In c-Jun knockout cells, JunB reduction induced p53-independent cell cycle arrest and apoptosis.
  • Combined JunB knockdown and c-Jun/JNK inactivation in B16-F10 cells led to apoptosis and extended mouse survival.

Conclusions:

  • JunB can function as a tumor promoter in the absence of c-Jun.
  • Simultaneous inactivation of c-Jun and JunB presents a potential therapeutic strategy for cancer intervention.