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Updated: Feb 25, 2026
Isolation of Cancer Stem Cells From Human Prostate Cancer Samples
Published on: March 14, 2014
Targeting Apoptotic Activity Against Prostate Cancer Stem Cells
Dagmara Jaworska1, Ewelina Szliszka2
1Department of Microbiology and Immunology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia in Katowice, Jordana 19, 41-808 Zabrze, Poland. djaworska@sum.edu.pl.
Abstract:
Numerous data suggest that an increase of cancer stem cells (CSCs) in tumor mass can be the reason for failure of conventional therapies because of their resistance. CD44+/CD24- cells are a putative cancer stem cells subpopulation in prostate cancer. TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) is an activator of apoptosis in tumor cells. However, some tumors are TRAIL-resistant. Cancer cells can be re-sensitized to TRAIL induced apoptosis by a combination of TRAIL and taxanes. The aim of this work was to analyze the enhancement of the anticancer effect of TRAIL by paclitaxel, cabazitaxel and docetaxel in the whole population of PC3 and DU145 prostate cancer cells, but also in CD44+/CD24- prostate cancer stem cells. We examined the apoptotic effect of TRAIL and taxanes using flow cytometry and Annexin-V-PE staining. The co-treatment with taxanes and TRAIL enhanced significantly the apoptosis in CD44+/CD24- cells only in PC3 cell line but not in DU145 cells. We discovered also that taxanes can increase the expression of death receptor TRAIL-R2 in PC3 prostate cancer cells. The results of our study show that treatment with paclitaxel, cabazitaxel and docetaxel is able to enhance the apoptosis induced by TRAIL even in prostate cancer stem cells.
Insights
Taxanes enhance the cancer-killing effects of TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) in prostate cancer stem cells. This combination therapy shows promise for overcoming treatment resistance in prostate cancer.
Area of Science:
- Oncology
- Cancer Biology
- Pharmacology
Background:
- Cancer stem cells (CSCs) contribute to therapy failure due to their resistance.
- CD44+/CD24- cells represent a potential CSC subpopulation in prostate cancer.
- Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis but faces resistance in some tumors.
Purpose of the Study:
- To investigate the combined effect of TRAIL and taxanes (paclitaxel, cabazitaxel, docetaxel) on prostate cancer cells, including CSCs.
- To determine if taxanes can re-sensitize prostate cancer cells and CSCs to TRAIL-induced apoptosis.
- To explore the impact of taxanes on TRAIL receptor expression.
Main Methods:
- Flow cytometry and Annexin-V-PE staining were used to assess apoptosis.
- The study analyzed both the general prostate cancer cell population (PC3, DU145) and the CD44+/CD24- CSC subpopulation.
- Expression levels of TRAIL-R2 were examined in PC3 cells.
Main Results:
- Co-treatment with taxanes and TRAIL significantly enhanced apoptosis in CD44+/CD24- cells of the PC3 cell line, but not DU145.
- Taxanes were found to increase the expression of the death receptor TRAIL-R2 in PC3 prostate cancer cells.
- The combination therapy demonstrated an enhanced apoptotic effect even in prostate cancer stem cells.
Conclusions:
- Paclitaxel, cabazitaxel, and docetaxel can enhance TRAIL-induced apoptosis in prostate cancer stem cells.
- This combination strategy holds potential for overcoming TRAIL resistance in prostate cancer.
- The findings suggest a viable therapeutic approach targeting CSCs in prostate cancer treatment.
