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Updated: Nov 21, 2025
07:16
Isolation of Cancer Stem Cells From Human Prostate Cancer Samples
Published on: March 14, 2014
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CD117/c-kit defines a prostate CSC-like subpopulation driving progression and TKI resistance
Koran S Harris1, Lihong Shi1, Brittni M Foster1
1Department of Cancer Biology, Wake Forest School of Medicine, Medical Center Blvd, Winston-Salem, NC, 27157, USA.
Scientific Reports
|January 15, 2021
Summary
CD117 expression in prostate cancer cells promotes aggressiveness and metastasis by enhancing cancer stem cell (CSC) traits. Blocking CD117 activation with TKIs may reduce progression, offering therapeutic insights.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Cancer stem-like cells (CSCs) drive tumor progression, metastasis, and recurrence.
- Circulating tumor cells (CTCs) may include CSCs, with CD117 (c-kit) identified in advanced prostate cancer CTCs.
- The role of CD117 expression and activation in prostate cancer aggressiveness and migration was previously unclear.
Purpose of the Study:
- To investigate the functional role of CD117 expression and activation in prostate cancer aggressiveness.
- To determine if CD117+ cells represent a cancer stem cell (CSC) population in prostate cancer.
- To explore the impact of CD117 signaling on proliferation, migration, stemness, and therapeutic resistance.
Main Methods:
- Analysis of CD117 expression and phosphorylation in relation to patient survival and Gleason grade.
- Utilized prostate cancer cell lines (C4-2, PC3-mm) with CD117+ subpopulations.
- Assessed cell proliferation, migration, prostasphere formation, and stemness marker expression.
- Employed xenograft limiting dilution and serial tumor initiation assays to identify CSCs.
- Investigated the effects of stem cell factor (SCF) stimulation and tyrosine kinase inhibitor (TKI) blockade on CD117+ cells.
Main Results:
- CD117 expression correlated with decreased overall and progression-free survival and increased Gleason grade.
- CD117+ prostate cancer cells exhibited enhanced proliferation, migration, and prostasphere formation.
- CD117+ cells demonstrated increased stemness gene expression and functioned as CSCs in vivo.
- SCF-mediated CD117 activation increased proliferation and invasiveness; TKI treatment context-dependently reduced progression.
Conclusions:
- CD117 expression and activation promote prostate cancer aggressiveness by driving the CSC phenotype.
- CD117 signaling contributes to tumor initiation, metastasis, and potentially TKI resistance.
- Targeting CD117 signaling represents a potential therapeutic strategy for advanced prostate cancer.
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