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Updated: Jun 23, 2026

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Tranilast inhibits hormone refractory prostate cancer cell proliferation and suppresses transforming growth factor
Kouji Izumi1, Atsushi Mizokami, You Qiang Li
1Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Ishikawa 920-8641, Japan.
Background:
Tranilast is a therapeutic agent used in treatment of allergic diseases, although it has been reported to show anti-tumor effects on some cancer cells. To elucidate the effects of tranilast on prostate cancer, we investigated the mechanisms of its anti-tumor effect on prostate cancer.
Methods:
The anti-tumor effects and related mechanisms of tranilast were investigated both in vitro on prostate cancer cell lines and bone-derived stromal cells, and in vivo on severe combined immunodeficient (SCID) mice. We verified its clinical effect in patients with advanced hormone refractory prostate cancer (HRPC).
Results:
Tranilast inhibited the proliferation of LNCaP, LNCaP-SF, and PC-3 cells in a dose-dependent manner and growth of the tumor formed by inoculation of LNCaP-SF in the dorsal subcutis and in the tibia of castrated SCID mice. Flow cytometry and TUNEL assay revealed induction of cell cycle arrest and apoptosis by tranilast. Tranilast increased expression of proteins involved in induction of cell cycle arrest and apoptosis. Coculture with bone-derived stromal cells induced proliferation of LNCaP-SF cells. Tranilast also suppressed secretion of transforming growth factor beta1 (TGF-beta1) from bone-derived stromal cells, which induced their differentiation. Moreover, tranilast inhibited TGF-beta1-mediated differentiation of bone-derived stromal cells and LNCaP-SF cell migration induced by osteopontin. In the clinical investigation, PSA progression was inhibited in 4 of 16 patients with advanced HRPC.
Conclusions:
These observations suggest that tranilast may be a useful therapeutic agent for treatment of HRPC via the direct inhibitory effect on cancer cells and suppression of TGF-beta1-associated osteoblastic changes in bone metastasis.
Insights
Tranilast shows anti-tumor effects on prostate cancer by inhibiting cell proliferation and inducing apoptosis. It also suppresses bone metastasis-related factors, suggesting its potential for treating hormone-refractory prostate cancer (HRPC).
Area of Science:
- Oncology
- Pharmacology
- Cancer Biology
Background:
- Tranilast, an anti-allergic agent, exhibits anti-tumor properties.
- Prostate cancer treatment remains a significant challenge, especially in advanced stages.
Purpose of the Study:
- To investigate the anti-tumor mechanisms of tranilast in prostate cancer.
- To evaluate tranilast's efficacy in hormone-refractory prostate cancer (HRPC).
Main Methods:
- In vitro studies on prostate cancer cell lines and bone-derived stromal cells.
- In vivo studies using severe combined immunodeficient (SCID) mice models.
- Clinical investigation in patients with advanced HRPC.
Main Results:
- Tranilast inhibited prostate cancer cell proliferation and induced cell cycle arrest and apoptosis.
- Tranilast suppressed transforming growth factor beta1 (TGF-beta1) secretion from bone-derived stromal cells.
- Clinical trials showed inhibition of PSA progression in HRPC patients.
Conclusions:
- Tranilast demonstrates direct anti-cancer effects on prostate cancer cells.
- Tranilast may mitigate bone metastasis by inhibiting TGF-beta1-associated osteoblastic changes.
- Tranilast shows promise as a therapeutic agent for HRPC.
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