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Updated: Sep 12, 2025
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TMEFF2 promotes hyperplastic prostate progression by degrading BAX via TRIM17
Mingzhou Li1, Daoquan Liu2, Yuting Bai3
1Department of Urology, Affiliated Hospital of Zunyi Medical University, 563000 Zunyi, China; Zhongnan Hospital of Wuhan University, 430071 Wuhan, China.
Cellular Signalling
|August 8, 2025
Summary
Tumor necrosis factor, epiregulin, and factor 2 (TMEFF2) promotes benign prostatic hyperplasia (BPH) by preventing BAX protein degradation. Targeting the TMEFF2-BAX pathway offers a new therapeutic strategy for BPH.
Area of Science:
- Urology
- Molecular Biology
- Oncology
Background:
- Benign prostatic hyperplasia (BPH) is a common condition in aging males, causing lower urinary tract symptoms (LUTS).
- The precise molecular mechanisms driving BPH development remain unclear.
- This study investigates the role of TMEFF2 in the pathogenesis of prostatic hyperplasia.
Purpose of the Study:
- To elucidate the functional role and molecular mechanisms of TMEFF2 in benign prostatic hyperplasia.
- To determine if TMEFF2 could serve as a therapeutic target for BPH.
Main Methods:
- Utilized human prostate tissues, cell lines, and a rat BPH model.
- Employed techniques including immunohistochemistry, qRT-PCR, Western blotting, and ubiquitination assays.
- Investigated TMEFF2's interaction with BAX and its role in BAX protein degradation.
Main Results:
- TMEFF2 expression is upregulated in BPH and correlates with prostate volume.
- TMEFF2 depletion inhibits proliferation, induces apoptosis, and reduces migration in BPH models.
- TMEFF2 facilitates BAX degradation via TRIM17-mediated ubiquitination, promoting BPH progression.
Conclusions:
- The TMEFF2-BAX signaling axis is a key driver of benign prostatic hyperplasia.
- TMEFF2 represents a promising therapeutic target for the treatment of BPH.
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