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- Title
Cucurbitacin E Induces G<sub>2</sub>/M Phase Arrest through STAT3/p53/p21 Signaling and Provokes Apoptosis via Fas/CD95 and Mitochondria-Dependent Pathways in Human Bladder Cancer T24 Cells.
- Authors
Wen-Wen Huang; Jai-Sing Yang; Meng-Wei Lin; Po-Yuan Chen; Shang- Ming Chiou; Fu-Shin Chueh; Yu-Hsuan Lan; Shu-Jen Pai; Tsuzuki, Minoru; Wai-Jane Ho; Jing-Gung Chung
- Abstract
Cucurbitacin E, a tetracyclic triterpenes compound extracted from cucurbitaceous plants, has been shown to exhibit anticancer and anti-inflammatory activities. The purpose of this study was to elucidate whether cucurbitacin E promotes cell cycle arrest and induces apoptosis in T24 cells and further to explore the underlying molecular mechanisms. The effects of cucurbitacin E on T24 cell's growth and accompanied morphological changes were examined by MTT assay and a phase-contrast microscope. DNA content, mitochondrial membrane potential (ΔΨm) and annexin V/PI staining were determined by flow cytometry. The protein levels were measured byWestern blotting. Our results demonstrated that cucurbitacin E-induced G2/ M arrest was associated with a marked increase in the levels of p53, p21 and a decrease in phospho-signal transducer and activator of transcription 3 (STAT3), cyclin-dependent kinase 1 (CDK1) and cyclin B. Cucurbitacin E-triggered apoptosis was accompanied with up-regulation of Fas/CD95, truncated BID (t-BID) and a loss of ΔΨm, resulting in the releases of cytochrome c, apoptotic protease activating factor 1 (Apaf-1) and apoptosis-inducing factor (AIF), and sequential activation of caspase-8, caspase-9, and caspase-3. Our findings provided the first evidence that STAT3/p53/p21 signaling, Fas/CD95 and mitochondria-dependent pathways play critical roles in cucurbitacin E-induced G2/ M phase arrest and apoptosis of T24 cells.
- Publication
Evidence-based Complementary & Alternative Medicine (eCAM), 2012, Vol 2012, p1
- ISSN
1741-427X
- Publication type
Academic Journal
- DOI
10.1155/2012/952762