| Literature DB >> 24384411 |
Xuan Yuan1, Tao Li1, Erlong Xiao1, Hong Zhao2, Yongqian Li1, Shengjun Fu1, Lu Gan3, Zhenhua Wang4, Qiusheng Zheng5, Zhiping Wang6.
Abstract
To examine the mechanisms by which licochalcone B (LCB) inhibits the proliferation of human malignant bladder cancer cell lines (T24 and EJ) in vitro and antitumor activity in vivo in MB49 (murine bladder cancer cell line) tumor model. Exposure of T24 or EJ cells to LCB significantly inhibited cell lines proliferation in a concentration-dependent and time-dependent manner, and resulted in S phase arrest in T24 or EJ cells, respectively. LCB treatment decreased the expression of cyclin A, cyclin-dependent kinase (CDK1 and CDK2) mRNA, cell division cycle 25 (Cdc25A and Cdc25B) protein. In addition, LCB treatment down-regulated Bcl-2 and survivin expression, enhanced Bax expression, activated caspase-3 and cleaved poly (ADP-ribose) polymerase (PARP) protein. Consistently, the tumorigenicity of LCB-treated MB49 cells was limited significantly by using the colony formation assay in vitro and the MB49 tumor model performed in C57BL/6 mice in vivo. These findings provide support for the use of LCB in chemoprevention and bladder cancer therapy.Entities:
Keywords: Apoptosis; Bladder cancer; Licochalcone B; S phase arrest
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Year: 2013 PMID: 24384411 DOI: 10.1016/j.fct.2013.12.030
Source DB: PubMed Journal: Food Chem Toxicol ISSN: 0278-6915 Impact factor: 6.023