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Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
Published on: June 7, 2019
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Oncogenic BRAF-Mediated Melanoma Cell Invasion
Hezhe Lu1, Shujing Liu2, Gao Zhang3
1Department of Biology, School of Arts and Sciences, University of Pennsylvania, Philadelphia, PA 19104, USA.
Cell Reports
|May 24, 2016
Summary
BRAF(V600E) mutation drives melanoma cell invasion and metastasis by promoting actin dynamics and matrix degradation. Inhibiting this mutation blocks invasion, suggesting a new therapeutic strategy for melanoma patients.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Melanoma patients with BRAF(V600E) mutations often have poor prognoses.
- The role of BRAF(V600E) in melanoma tumorigenesis is known, but its role in metastasis is debated.
Purpose of the Study:
- To investigate the role of BRAF(V600E) in melanoma cell invasion and metastasis.
- To explore BRAF(V600E) as a therapeutic target for inhibiting melanoma spread.
Main Methods:
- Assessing melanoma cell invasion via F-actin and cortactin foci formation and extracellular matrix degradation.
- Utilizing a BRAF(V600E)-driven murine melanoma model and human tumor biopsies.
- Performing genome-wide expression analysis and Western blotting to study protein phosphorylation.
Main Results:
- BRAF(V600E) melanoma cells exhibit significant invasion activity, mediated by F-actin and cortactin foci.
- Inhibition of BRAF(V600E) effectively blocks melanoma cell invasion in vitro and in vivo.
- BRAF(V600E) signaling, through ERK, phosphorylates cortactin and Exo70, regulating actin dynamics and matrix metalloprotease secretion.
Conclusions:
- BRAF(V600E) plays a crucial role in melanoma cell invasion and metastasis.
- Targeting BRAF(V600E) and downstream signaling pathways offers a potential therapeutic strategy to inhibit melanoma spread.
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