These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: [Effects of selective cyclooxygenase-2 inhibitor on proliferation and apoptosis of human bladder cancer cell line T24]. Author: Zhang J, Xu ZQ, Hu Q, Qiu XW, Wang ZR. Journal: Ai Zheng; 2007 Apr; 26(4):377-81. PubMed ID: 17430655. Abstract: BACKGROUND & OBJECTIVE: Cyclooxygenase-2 (COX-2) is related closely to the tumorigenesis of bladder cancer, and COX-2 inhibitor has potential antitumor effect. This study was to investigate the effects of selective COX-2 inhibitors on the proliferation and apoptosis of human bladder cancer cell line T24. METHODS: The effects of selective COX-2 inhibitors SC-58125 and celecoxib, and nonselective COX inhibitor indomethacin on the proliferation of T24 cells were evaluated by MTT assay. Cell apoptosis was determined by flow cytometry (FCM), DNA ladder electrophoresis, and fluorescent microscopy with Hoechst33258 staining. The expression of apoptosis-related genes Bcl-2 and Bax were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Within concentrations of 12.5-200 micromol/L, SC-58125, celecoxib, and indomethacin could inhibit the proliferation of T24 cells to different extents. SC-58125 tended to be more effective than the other two. The 50% inhibition concentration (IC50) of SC-58125 was determined to be 25-50 micromol/L. The apoptosis of T24 cells was enhanced after exposure to SC-58125. When treated with 100 micromol/L SC-58125 for 6 and 12 h, the apoptosis rates of T24 cells were (7.95+/-1.88)% and (12.5+/-2.42)%, respectively, which were significantly higher than that of control cells (P<0.05). But the expression of Bcl-2 and Bax genes did not change. CONCLUSIONS: Selective COX-2 inhibitor could inhibit the proliferation and induce the apoptosis of T24 cells.[Abstract] [Full Text] [Related] [New Search]