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Transmembrane protein 64 modulates prostate tumor progression by regulating Wnt3a secretion
Yeon Hee Moon1, Wonbong Lim2,3,4, Byung-Chul Jeong2,3
1Department of Dental Hygiene, Chodang University, Muangun, Jeollanamdo 58530, Republic of Korea.
Oncology Letters
|July 11, 2019
Summary
Transmembrane protein 64 (Tmem64) regulates Wnt3a secretion in prostate cancer. Tmem64 downregulation promotes Wnt3a secretion, potentially driving metastatic progression and therapy resistance.
Area of Science:
- Molecular Biology
- Cancer Research
- Cell Signaling
Background:
- Wnt signaling is crucial in the prostate tumor microenvironment, influencing therapy resistance.
- Wnt3a, a key ligand, requires specific factors for bioactive production, whose functions remain unclear.
- Transmembrane protein 64 (Tmem64) was previously identified as a regulator of Wnt/β-catenin signaling.
Purpose of the Study:
- To investigate the role of Tmem64 in prostate cancer cells.
- To elucidate Tmem64's mechanism in regulating Wnt3a secretion and its impact on metastasis.
Main Methods:
- Modulating Tmem64 expression (overexpression and mutation) in prostate cancer cells.
- Assessing Wnt3a secretion and Lef/Tcf-sensitive transcription.
- Analyzing Tmem64 and Wnt3a expression in cell lines (PC3, LNCaP, DU145) and a mouse metastasis model.
Main Results:
- Tmem64 overexpression inhibited Wnt3a secretion and downstream transcription.
- A Tmem64 transmembrane domain deletion mutant restored Wnt3a secretion.
- PC3 cells showed higher Tmem64 expression than LNCaP and DU145 cells.
- In vivo, Tmem64 was downregulated in metastatic lesions, while Wnt3a was upregulated.
Conclusions:
- Tmem64 acts as an inhibitor of Wnt3a secretion in prostate cancer cells.
- Tmem64 downregulation correlates with increased Wnt3a, suggesting a role in prostate cancer metastasis.
- Tmem64 is a potential therapeutic target for managing prostate cancer progression.
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