Although UV is known to induce apoptotic cell death to various animal cells, relationship between cell cycle and UV-induced apoptosis is still unclear. In this study, we investigated the role of G1 phase in UV-induced apoptosis by using EL-4 mouse lymphoma cells which have wild type p53. After 500 J/m2 UV irradiation, an increase of apoptotic fraction was accompanied by cell cycle accumulation in the G1 phase.
View Article and Find Full Text PDFWe previously reported that mouse mammary carcinoma cell lines (MMT060562 and BALB/c-MC) induced osteoclast formation through production of prostaglandin E2 (PGE2) in cocultures with mouse bone marrow cells, but the mechanism(s) of PG production remained unclear. In the present in vitro and in vivo studies, we tested the involvement of cyclo-oxygenase-2 (COX-2), an inducible rate-limiting enzyme in PG biosynthesis, in the stimulation of osteoclast formation by mouse mammary carcinoma cell lines. Addition of a selective COX-2 inhibitor, JTE-522, to cocultures of mammary carcinoma cell lines and bone marrow cells lowered PGE2 concentration in the culture media and inhibited osteoclast formation in a dose-dependent manner.
View Article and Find Full Text PDFInt J Radiat Oncol Biol Phys
June 2000
Purpose: Apoptosis is currently being evaluated for its importance as a pathway of radiation-induced cell death. However, the difference in the mechanisms between premitotic and postmitotic apoptosis following X-irradiation remains not well understood. We show here that the human monoblastoid cell line U937 can be induced to undergo these two different types of apoptosis.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2000
The placenta-type isozyme of human 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (HP2K) is expressed in several tissues such as placenta, brain, testis, liver, kidney, skeletal muscle, and primary blood mononuclear cells. To better understand the regulation of HP2K gene expression, we isolated and characterized its genomic DNA, which includes the promoter region. The results of oligo-capping analysis indicate that the transcription start point (tsp) is an adenine residue 329 bp upstream of the translational start codon.
View Article and Find Full Text PDFCaffeine overrides checkpoints in the G2 phase of the cell cycle by inhibiting DNA repair at this phase and increases the cytotoxicity of antitumor drugs, such as cis-diamminedichloroplatinum (CDDP). The enhanced cell death induced by caffeine is characterized by apoptosis. In this paper, we demonstrate that this apoptotic event occurs in S phase of the cell cycle, whereas CDDP induces a block in G2/M.
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