 |
English
|
正體中文
|
简体中文
|
Items with full text/Total items : 12145/12927 (94%)
Visitors : 847609
Online Users : 330
|
|
|
Loading...
|
Please use this identifier to cite or link to this item:
http://ir.nhri.org.tw/handle/3990099045/6672
|
| Title: | Baicalein induces G1 arrest in oral cancer cells by enhancing the degradation of cyclin D1 and activating AhR to decrease Rb phosphorylation |
| Authors: | Cheng, YH;Li, LA;Lin, P;Cheng, LC;Hung, CH;Chang, NW;Lin, C |
| Contributors: | Division of Environmental Health and Occupational Medicine |
| Abstract: | Baicalein is a flavonoid, known to have anti-inflammatory and anti-cancer effects. As an aryl hydrocarbon receptor (AhR) ligand, baicalein at high concentrations blocks AhR-mediated dioxin toxicity. Because AhR had been reported to play a role in regulating the cell cycle, we suspected that the anti-cancer effect of baicalein is associated with AhR. This study investigated the molecular mechanism involved in the anti-cancer effect of baicalein in oral cancer cells HSC-3, including whether such effect would be AhR-mediated. Results revealed that baicalein inhibited cell proliferation and increased AhR activity in a dose-dependent manner. Cell cycle was arrested at the G1 phase and the expression of CDK4, cyclin D1, and phosphorylated retinoblastoma (pRb) was decreased. When the AhR was suppressed by siRNA, the reduction of pRb was partially reversed, accompanied by a decrease of cell population at G1 phase and an increase at S phase, while the reduction of cyclin D1 and CDK4 did not change. This finding suggests that the baicalein activation of AhR is indeed associated with the reduction of pRb, but is independent of the reduction of cyclin D1 and CDK4. When cells were pre-treated with LiCl, the inhibitor of GSK-3β, the decrease of cyclin D1 was blocked and the reduction of pRb was recovered. The data indicates that in HSC-3 the reduction of pRb is both mediated by baicalein through activation of AhR and facilitation of cyclin D1 degradation, which causes cell cycle arrest at the G1 phase, and results in the inhibition of cell proliferation. |
| Date: | 2012-09-15 |
| Relation: | Toxicology and Applied Pharmacology. 2012 Sep 15;263(3):360-367. |
| Link to: | http://dx.doi.org/10.1016/j.taap.2012.07.010 |
| JIF/Ranking 2023: | http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0041-008X&DestApp=IC2JCR |
| Cited Times(WOS): | https://www.webofscience.com/wos/woscc/full-record/WOS:000308682600012 |
| Cited Times(Scopus): | http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84865431008 |
| Appears in Collections: | [林嬪嬪] 期刊論文
[李立安] 期刊論文
|
Files in This Item:
| File |
Description |
Size | Format | |
|---|
| SCP84864150202.pdf | | 789Kb | Adobe PDF | 656 | View/Open |
|
All items in NHRI are protected by copyright, with all rights reserved.
|
