Related Experiment Video
Updated: Jul 30, 2025

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel
Published on: September 8, 2017
JMJD2A participates in cytoskeletal remodeling to regulate castration-resistant prostate cancer docetaxel resistance
Xiang Cai1, Xi Duan2, Tielong Tang1
1Department of Urology, Affiliated Hospital of North Sichuan Medical College, No. 1 Maoyuan South Road, Sichuan, 637000, Nanchong, China.
Background:
To investigate underlying mechanism of JMJD2A in regulating cytoskeleton remodeling in castration-resistant prostate cancer (CRPC) resistant to docetaxel.
Methods:
Tissue samples from CRPC patients were collected, and the expression of JMJD2A, miR-34a and cytoskeleton remodeling-related proteins were evaluated by qPCR, western blot and immunohistochemistry, and pathological changes were observed by H&E staining. Further, JMJD2A, STMN1 and TUBB3 were knocked down using shRNA in CRPC cell lines, and cell viability, apoptosis and western blot assays were performed. The interaction between miR-34a/STMN1/β3-Tubulin was analyzed with dual-luciferase reporter and co-immunoprecipitation assays.
Results:
In clinical experiment, the CRPC-resistant group showed higher expression of JMJD2A, STMN1, α-Tubulin, β-Tubulin and F-actin, and lower expression of miR-34a and β3-Tubulin compared to the sensitive group. In vitro experiments showed that JMJD2A could regulate cytoskeletal remodeling through the miR-34a/STMN1/β3-Tubulin axis. The expression of miR-34a was elevated after knocking down JMJD2A, and miR-34a targeted STMN1. The overexpression of miR-34a was associated with a decreased expression of STMN1 and elevated expression of β3-Tubulin, which led to the disruption of the microtubule network, decreased cancer cell proliferation, cell cycle arrest in the G0/G1 phase, and increased apoptosis.
Conclusion:
JMJD2A promoted docetaxel resistance in prostate cancer cells by regulating cytoskeleton remodeling through the miR-34a/STMN1/β3-Tubulin axis.
Insights
JMJD2A promotes docetaxel resistance in prostate cancer by altering cytoskeleton remodeling via the miR-34a/STMN1/β3-Tubulin pathway, impacting cell proliferation and apoptosis.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Castration-resistant prostate cancer (CRPC) often develops resistance to docetaxel chemotherapy.
- The underlying mechanisms of docetaxel resistance, particularly involving cytoskeleton remodeling, require further investigation.
Purpose of the Study:
- To elucidate the role of JMJD2A in regulating cytoskeleton remodeling in docetaxel-resistant CRPC.
- To identify the molecular pathway, including microRNA and protein interactions, through which JMJD2A exerts its effects.
Main Methods:
- Analysis of JMJD2A, miR-34a, and cytoskeleton-related protein expression in CRPC patient tissues.
- In vitro studies involving knockdown of JMJD2A, STMN1, and TUBB3 in CRPC cell lines.
- Assessment of cell viability, apoptosis, and molecular interactions using qPCR, western blot, dual-luciferase reporter, and co-immunoprecipitation assays.
Main Results:
- Higher JMJD2A and STMN1 expression, with lower miR-34a and β3-Tubulin, observed in docetaxel-resistant CRPC.
- JMJD2A regulates cytoskeletal remodeling via the miR-34a/STMN1/β3-Tubulin axis.
- miR-34a overexpression led to decreased STMN1, increased β3-Tubulin, microtubule disruption, reduced proliferation, G0/G1 cell cycle arrest, and enhanced apoptosis.
Conclusions:
- JMJD2A promotes docetaxel resistance in prostate cancer.
- The miR-34a/STMN1/β3-Tubulin axis is a key mediator of JMJD2A-induced cytoskeleton remodeling and chemoresistance.
- Targeting JMJD2A or modulating this axis may offer therapeutic strategies for overcoming docetaxel resistance in CRPC.
More Related Videos
Related Concept Videos
Abnormal Proliferation
Drugs that Stabilize Microtubules
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Destabilization of Microtubules
Cancer Stem Cells and Tumor Maintenance
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
The JAK-STAT Signaling Pathway

