Related Experiment Video

Updated: Jan 21, 2026

Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma
08:18

Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma

Published on: September 8, 2021

3.3K

C-Jun drives melanoma progression in PTEN wild type melanoma cells

Melanie Kappelmann-Fenzl1,2, Claudia Gebhard3,4, Alexander O Matthies1

  • 1Institute of Biochemistry (Emil-Fischer Center), Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.

Cell Death & Disease
|August 6, 2019
PubMed

Insights

Activating transcription factor AP-1, specifically c-Jun, drives melanoma by altering cancer pathways like MAPK and PI3K. Targeting c-Jun may inhibit melanoma cell survival, especially in PTEN-positive tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Activating Protein 1 (AP-1) transcription factors, particularly c-Jun, play a crucial role in melanoma progression.
  • Identifying AP-1 target genes is essential for understanding and inhibiting oncogenic signaling in melanoma.

Purpose of the Study:

  • To map genome-wide c-Jun occupancy in melanoma cells.
  • To identify c-Jun-regulated genes and their role in cancer-relevant signaling pathways.
  • To investigate the dependency of c-Jun's importance on melanoma stage and PTEN mutation status.

Main Methods:

  • Genome-wide c-Jun occupancy mapping in melanoma cells.
  • Correlation of AP-1 binding data with transcriptome data.
  • Analysis of c-Jun's role in mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3K) pathways.
  • Assessment of c-Jun's relevance in different melanoma stages and PTEN mutation contexts.

Main Results:

  • c-Jun promotes the malignant melanoma phenotype by deregulating genes in MAPK and PI3K signaling pathways.
  • The significance of c-Jun is dependent on melanoma stage and the mutation status of the tumor suppressor PTEN.
  • c-Jun activation overrides PTEN's tumor-suppressive effects during early melanoma development.

Conclusions:

  • c-Jun is a key regulator of melanoma cell survival and malignant phenotype, particularly through its influence on MAPK and PI3K pathways.
  • Targeting c-Jun in PTEN-positive melanoma cells presents a potential therapeutic strategy to prevent melanoma cell survival and metastasis.
  • Understanding c-Jun's role in specific melanoma contexts, like PTEN status, is crucial for developing effective treatments.

More Related Videos

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis07:41

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis

Published on: March 8, 2022

2.8K
The Three-Dimensional Human Skin Reconstruct Model: a Tool to Study Normal Skin and Melanoma Progression11:02

The Three-Dimensional Human Skin Reconstruct Model: a Tool to Study Normal Skin and Melanoma Progression

Published on: August 3, 2011

50.8K

Related Concept Videos

Energy to Drive Translocation01:37

Energy to Drive Translocation

Mitochondrial protein import is powered by two distinct energy sources: ATP hydrolysis and electrochemical potential across the inner membrane. Newly synthesized precursors are bound by cytosolic chaperones of the Hsp70 family, which guide them to the import receptors on the mitochondrial surface. Utilizing the energy of ATP hydrolysis, Hsp70 chaperones transfer these precursors to the TOM receptors on the mitochondrial outer membrane.
Generally, polypeptides are unfolded by two distinct...
2.7K
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
6.4K
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
7.2K
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
2.2K
Connective Tissue Cell Types01:22

Connective Tissue Cell Types

Connective tissue develops from the mesoderm of a developing embryo and consists of cells, fibers, and ground substance: a gel-like material containing large complexes of carbohydrates and proteins. Connective tissue was first identified as a separate tissue family in the 18th century, and Johannes Peter Muller coined the term connective tissue.
Fat cells (adipocytes), smooth muscle cells (myoblasts), and bone cells (osteoblasts) are some connective tissue cell types. Some immune system cells...
4.1K
Types of Receptors: Cell Surface Receptors01:28

Types of Receptors: Cell Surface Receptors

Cell-surface receptors, also known as transmembrane receptors, are cell surface, membrane-anchored (integral) proteins that bind to external ligand molecules. This type of receptor spans the plasma membrane and performs signal transduction, converting an extracellular signal into an intracellular signal. Ligands that interact with cell-surface receptors do not have to enter the cell that they affect. Cell-surface receptors are also called cell-specific proteins or markers because they are...
26.8K