Medicarpin induces G1 arrest and mitochondria-mediated intrinsic apoptotic pathway in bladder cancer cells
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Updated: Jul 26, 2025
Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
Published on: October 30, 2013
Yuan Chen1,2, Liqi Yin1, Mingxuan Hao1
11College of Life Science and Technology, Innovation Center of Molecular Diagnostics, Beijing University of Chemical Technology, Beijing 100029, China.
Abstract:
Bladder cancer (BC) is the tenth most commonly diagnosed cancer. High recurrence, chemoresistance, and low response rate hinder the effective treatment of BC. Hence, a novel therapeutic strategy in the clinical management of BC is urgently needed. Medicarpin (MED), an isoflavone from Dalbergia odorifera, can promote bone mass gain and kill tumor cells, but its anti-BC effect remains obscure. This study reve aled that MED effectively inhibited the proliferation and arrested the cell cycle at the G1 phase of BC cell lines T24 and EJ-1 in vitro. In addition, MED could significantly suppress the tumor growth of BC cells in vivo. Mechanically, MED induced cell apoptosis by upregulating pro-apoptotic proteins BAK1, Bcl2-L-11, and caspase-3. Our data suggest that MED suppresses BC cell growth in vitro and in vivo via regulating mitochondria-mediated intrinsic apoptotic pathways, which can serve as a promising candidate for BC therapy.
Insights
Medicarpin (MED) effectively inhibits bladder cancer (BC) cell growth and tumor development. This natural compound induces apoptosis through mitochondria-mediated pathways, showing promise for BC therapy.
Area of Science:
- Oncology
- Pharmacology
- Natural Products
Background:
- Bladder cancer (BC) presents significant treatment challenges due to high recurrence rates and chemoresistance.
- Novel therapeutic strategies are crucial for improving clinical management of BC.
- Medicarpin (MED), an isoflavone from *Dalbergia odorifera*, has shown anti-tumor potential but its effect on BC is unknown.
Purpose of the Study:
- To investigate the anti-cancer effects of Medicarpin (MED) on bladder cancer (BC) cells.
- To elucidate the underlying mechanisms of MED's action on BC cell proliferation and apoptosis.
Main Methods:
- *In vitro* studies using BC cell lines (T24 and EJ-1) to assess proliferation and cell cycle arrest.
- *In vivo* studies to evaluate tumor growth suppression in BC models.
- Western blot analysis to examine the expression of apoptosis-related proteins.
Main Results:
- MED significantly inhibited proliferation and induced G1 phase cell cycle arrest in BC cell lines *in vitro*.
- MED demonstrated significant suppression of BC tumor growth *in vivo*.
- MED upregulated pro-apoptotic proteins (BAK1, Bcl2-L-11, caspase-3), indicating activation of intrinsic apoptotic pathways.
Conclusions:
- MED effectively suppresses bladder cancer cell growth both *in vitro* and *in vivo*.
- The anti-cancer mechanism involves the regulation of mitochondria-mediated intrinsic apoptotic pathways.
- Medicarpin (MED) represents a promising therapeutic candidate for bladder cancer treatment.
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