Cellular Effects of Troglitazone on YD15 Tongue Carcinoma Cells.
10.11620/IJOB.2016.41.3.113
- Author:
Loan TA THI
1
;
Hoon YOO
Author Information
1. Department of Pharmacology and Dental Therapeutics, College of Dentistry, Chosun University, Gwangju 501-759 South Korea. hoon_yoo@chosun.ac.kr
- Publication Type:Original Article
- Keywords:
Cell cycle arrest;
apoptosis;
troglitazone;
YD15 tongue carcinoma
- MeSH:
Apoptosis;
Blotting, Western;
Caspase 3;
Caspase 7;
Cell Cycle Checkpoints;
Cell Cycle Proteins;
Cyclin A;
Cyclin B1;
Cyclin D1;
Cyclins;
Flow Cytometry;
Peroxisomes;
Tongue*;
Up-Regulation
- From:International Journal of Oral Biology
2016;41(3):113-118
- CountryRepublic of Korea
- Language:English
-
Abstract:
An FDA approved drug for the treatment of type II diabetes, Troglitazone (TRO), a peroxisome proliferator–activated receptor gamma agonist, is withdrawn due to severe idiosyncratic hepatotoxicity. In the search for new applications of TRO, we investigated the cellular effects of TRO on YD15 tongue carcinoma cells. TRO suppressed the growth of YD15 cells in the MTT assay. The inhibition of cell growth was accompanied by the induction of cell cycle arrest at G₀/G₁ and apoptosis, which are confirmed by flow cytometry and western blotting. TRO also suppressed the expression of cell cycle proteins such as cyclin D1, cdk2, cdk4, cyclin B1, cdk1(or cdc2), cyclin E1 and cyclin A. The inhibition of cell cycle proteins was coincident with the up-regulation of p21(CIP1/WAF1) and p27(KIP1). In addition, TRO induces the activation of caspase-3 and caspase-7, as well as the cleavage of PARP. Further, TRO suppressed the expressions of Bcl-2 without affecting the expressions of Bad and Bax. Overall, our data supports that TRO induces cell cycle arrest and apoptosis on YD15 cells.