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Isolation of Cancer Stem Cells From Human Prostate Cancer Samples
Published on: March 14, 2014
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The stem cell factor (SCF)/c-KIT signalling in testis and prostate cancer
Henrique J Cardoso1, Marília I Figueira1, Sílvia Socorro2
1CICS-UBI, Centro de Investigação em Ciências da Saúde, Universidade da Beira Interior, Av. Infante D. Henrique, 6200-506, Covilhã, Portugal.
Journal of Cell Communication and Signaling
|June 29, 2017
Summary
Stem cell factor (SCF) binding to c-KIT activates pathways promoting cell growth. Inhibiting c-KIT shows promise for treating testicular and prostate cancers by targeting abnormal cell proliferation.
Area of Science:
- Molecular Biology
- Oncology
- Cell Signaling
Background:
- Stem cell factor (SCF) interacts with the tyrosine kinase receptor c-KIT, initiating signaling cascades.
- SCF/c-KIT signaling regulates crucial cellular processes like proliferation, apoptosis, differentiation, and migration.
- Aberrant c-KIT activation, through mutations or overexpression, is implicated in various cancers.
Purpose of the Study:
- To review signaling pathways activated by the SCF/c-KIT system.
- To discuss the therapeutic potential of c-KIT inhibitors in male cancers.
- To highlight tr-KIT as a specific drug target in prostate cancer.
Main Methods:
- Literature review of SCF/c-KIT signaling pathways.
- Analysis of c-KIT's role in testicular and prostatic cancers.
- Discussion of c-KIT inhibitors as a treatment strategy.
Main Results:
- SCF/c-KIT signaling involves PI3-K, Src, JAK/STAT, PLC-γ, and MAPK pathways.
- Overactivated c-KIT drives proliferation in male cancers, particularly via PI3-K and Src pathways.
- Truncated c-KIT (tr-KIT) is crucial for Src activity in prostate cancer.
Conclusions:
- Targeting the SCF/c-KIT pathway offers a potential therapeutic strategy for male cancers.
- c-KIT inhibitors may be effective in treating testicular and prostate cancers.
- The tumor-specific tr-KIT variant presents a promising target for novel drug development.
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