Medicarpin induces G1 arrest and mitochondria-mediated intrinsic apoptotic pathway in bladder cancer cells.
Yuan ChenLiqi YinMingxuan HaoWenkai XuJixian GaoYuxin SunQiao WangShi ChenYoufeng LiangRui GuoJinku ZhangJinmei LiQiongli ZhaiRunfen ChengJiansong WangHaifeng WangZhao YangPublished in: Acta pharmaceutica (Zagreb, Croatia) (2023)
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.
Keyphrases
- cell death
- cell cycle
- cell cycle arrest
- cell proliferation
- induced apoptosis
- anti inflammatory
- signaling pathway
- bone mineral density
- spinal cord injury
- stem cells
- artificial intelligence
- squamous cell carcinoma
- diabetic rats
- mesenchymal stem cells
- deep learning
- drug induced
- cell therapy
- combination therapy
- endothelial cells