How a protein complex helps genetic messages leave cells in advanced prostate cancer
Official title: Function of the METTL3-NUP93 complex-mediated nuclear export of m6A-modified mRNAs in castration-resistant prostate cancer.
Funded at University of Virginia · NIH-11285441 · Data updated 2026-11-12
This project looks at whether blocking a protein complex that helps send genetic messages (mRNA) out of the cell nucleus can slow the growth and spread of castration‑resistant prostate cancer.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Virginia NIH-funded |
| Lab location | 1 site (Charlottesville, United States) |
| Project start | April 1, 2023 |
| Project end | January 31, 2029 |
| Funding year | 2026 |
| Award (this year) | $424,908 |
| NIH project number | 5R01CA279681-03 |
| Project ID | NIH-11285441 on NIH RePORTER |
Who could benefit from this research
✓Could help
Men with castration‑resistant or metastatic prostate cancer, especially those willing to provide tumor tissue for research, would be the most relevant candidates for involvement or future trials.
✕Less likely to help
People without prostate cancer or those seeking an immediate therapeutic benefit should not expect direct help from this laboratory‑focused project.
What this research studies
Researchers will examine tumor tissue and laboratory prostate cancer cells to study a protein complex called METTL3‑NUP93 that helps export m6A‑tagged mRNA from the nucleus. They will compare METTL3 and NUP93 levels in normal prostate tissue, primary tumors, and metastatic castration‑resistant prostate cancer using tissue staining. In lab-grown cancer cells they will disrupt the METTL3‑NUP93 interaction with targeted mutations and measure effects on cell growth and movement. Proteomics and molecular methods will track how changes in this complex affect mRNA export and cancer cell behavior.
Why it matters
Potential benefit: If successful, this work could reveal a new molecular target for treatments aimed at slowing or stopping castration‑resistant prostate cancer progression.
How similar studies have gone: Previous research has linked METTL3 and nucleoporins to cancer, but studying their interaction in mRNA export specifically in castration‑resistant prostate cancer is relatively novel.
Where this research is happening
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University of Virginia
Charlottesville, United States Active
Researchers
- Principal investigator: Xu, Kexin — University of Virginia
- Study coordinator: Xu, Kexin
Related research
Other NIH-funded projects on the same topics.
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Understanding how aggressive cell states emerge in castration-resistant prostate cancer
A research project aims to uncover the hidden cell states that help prostate cancer resist standard therapy and how these states arise early in tumor development.
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Enhancer RNA CYP11A1-eRNA in castration-resistant prostate cancer
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Targeted Immunostimulatory Dual Drug Conjugates for Heterogeneous Metastatic Prostate Cancer
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Androgen Receptor Action in Prostate Cancer that Stops Responding to Therapy
This grant supports research to understand why certain prostate cancers stop responding to AR-targeted therapies and to find new ways to target them.
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Hyperactive methylation in a hard-to-treat prostate cancer subtype
Researchers are studying a newly identified methylation-heavy group of advanced prostate cancer to understand its biology and find clues for better treatments.
-
Therapeutic Targeting of Lineage Plasticity in Advanced Prostate Cancer
A cancer research effort aimed at understanding and tackling how aggressive prostate cancers become resistant to standard AR-targeted therapies.
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.