JTE-522, a selective COX-2 inhibitor, inhibits cell proliferation and induces apoptosis in RL95-2 cells.
Abstract
AIM: To investigate whether JTE-522
[4-(4-cyclohexyl-2-methyloxazol-5-yl)-2-fluorobenzenesulfonamide], a selective
COX-2 inhibitor, can induce apoptosis and inhibit cell proliferation in human
endometrial cancer cell line RL95-2 cells and to explore the molecular
mechanisms.
METHODS: [3-(4,5)-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT),
DNA ladder, enzyme-linked immunosorbent assay (ELISA), flow cytometry, RT-PCR,
and Western blot analysis were employed to investigate effect of JTE-522 on human
endometrial cancer cell line RL95-2 cells and the related molecular mechanisms.
RESULTS: JTE-522 inhibited the growth of RL95-2 cells and induced the apoptosis.
Furthermore, it arrested G0/G1 phase and inhibited S phase in RL95-2 cells.
JTE-522 inhibited the expressions of COX-2 mRNA, phosphorylated Rb, and CDK4
proteins, while increased the levels of p53, p21, cyclin D1 proteins, and the
activity of caspase-3 in RL95-2 cells.
CONCLUSION: JTE-522 inhibits cell proliferation and induces apoptosis in RL95-2
cells, which may be associated with the activation of caspase-3-like proteases,
down-regulation of the expression of COX-2 mRNA, phosphorylated Rb, and CDK4
proteins, and up-regulation of the expressions of p53, p21, and cyclin D1
proteins.
Keywords:
[4-(4-cyclohexyl-2-methyloxazol-5-yl)-2-fluorobenzenesulfonamide], a selective
COX-2 inhibitor, can induce apoptosis and inhibit cell proliferation in human
endometrial cancer cell line RL95-2 cells and to explore the molecular
mechanisms.
METHODS: [3-(4,5)-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT),
DNA ladder, enzyme-linked immunosorbent assay (ELISA), flow cytometry, RT-PCR,
and Western blot analysis were employed to investigate effect of JTE-522 on human
endometrial cancer cell line RL95-2 cells and the related molecular mechanisms.
RESULTS: JTE-522 inhibited the growth of RL95-2 cells and induced the apoptosis.
Furthermore, it arrested G0/G1 phase and inhibited S phase in RL95-2 cells.
JTE-522 inhibited the expressions of COX-2 mRNA, phosphorylated Rb, and CDK4
proteins, while increased the levels of p53, p21, cyclin D1 proteins, and the
activity of caspase-3 in RL95-2 cells.
CONCLUSION: JTE-522 inhibits cell proliferation and induces apoptosis in RL95-2
cells, which may be associated with the activation of caspase-3-like proteases,
down-regulation of the expression of COX-2 mRNA, phosphorylated Rb, and CDK4
proteins, and up-regulation of the expressions of p53, p21, and cyclin D1
proteins.