Compounds > n(4)-oleylcytosine-arabinoside

n(4)-oleylcytosine-arabinoside and Prostatic-Neoplasms

n(4)-oleylcytosine-arabinoside has been researched along with Prostatic-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for n(4)-oleylcytosine-arabinoside and Prostatic-Neoplasms

Article	Year
The novel heterodinucleoside dimer 5-FdU-NOAC is a potent cytotoxic drug and a p53-independent inducer of apoptosis in the androgen-independent human prostate cancer cell lines PC-3 and DU-145. The Prostate, 2000, Sep-15, Volume: 45, Issue:1 We analyzed the cytotoxic properties of the new heterodinucleoside phosphate dimer 5-FdU-NOAC, which is composed of the cytotoxic drugs 5-FdU and N(4)-octadecyl-1-beta-D-arabinofuranosylcytosine (NOAC) against human prostate tumor cells.. 5-FdU-NOAC effects on cell proliferation, cell cycle distribution, thymidylate synthase activity, and apoptosis were investigated in vitro in the two human prostate carcinoma cell lines DU-145 and PC-3 and compared to cells treated with the corresponding single drugs 5-FdU and NOAC.. Treatment of the cells with 5-FdU-NOAC resulted in IC(50) values of 3.9-5 microM and in a complete inhibition of cell proliferation at 200 microM after 96 hr compared to 5-FdU, where 10% of the cells remained resistant. Flow cytometric analysis revealed cell cycle perturbations in S-phase only in the DU-145 cells. 5-FdU-NOAC caused 50% inhibition of thymidylate synthase after 90 min at 0.6 microM in both cell lines. Apoptotic cell fractions in DU-145 (66%) and in PC-3 (34%) cells were found after treatment with 5-FdU-NOAC for 96 hr. DNA fragmentation further confirmed the induction of apoptosis.. 5-FdU-NOAC inhibits thymidylate synthase and cell cycle progression causing proliferation arrest and apoptosis in DU-145 and PC-3 cells, suggesting a potential role of 5-FdU-NOAC for the treatment of prostate cancer. Topics: Androgens; Antimetabolites, Antineoplastic; Apoptosis; Biotransformation; Cell Cycle; Cell Division; Cytarabine; Dimerization; Dose-Response Relationship, Drug; Enzyme Inhibitors; Floxuridine; Fluorodeoxyuridylate; Humans; Hydrolysis; Male; Neoplasms, Hormone-Dependent; Phosphodiesterase I; Phosphoric Diester Hydrolases; Prodrugs; Prostatic Neoplasms; Thymidylate Synthase; Tumor Cells, Cultured; Tumor Suppressor Protein p53	2000

Article

Year

The novel heterodinucleoside dimer 5-FdU-NOAC is a potent cytotoxic drug and a p53-independent inducer of apoptosis in the androgen-independent human prostate cancer cell lines PC-3 and DU-145.

The Prostate, 2000, Sep-15, Volume: 45, Issue:1

We analyzed the cytotoxic properties of the new heterodinucleoside phosphate dimer 5-FdU-NOAC, which is composed of the cytotoxic drugs 5-FdU and N(4)-octadecyl-1-beta-D-arabinofuranosylcytosine (NOAC) against human prostate tumor cells.. 5-FdU-NOAC effects on cell proliferation, cell cycle distribution, thymidylate synthase activity, and apoptosis were investigated in vitro in the two human prostate carcinoma cell lines DU-145 and PC-3 and compared to cells treated with the corresponding single drugs 5-FdU and NOAC.. Treatment of the cells with 5-FdU-NOAC resulted in IC(50) values of 3.9-5 microM and in a complete inhibition of cell proliferation at 200 microM after 96 hr compared to 5-FdU, where 10% of the cells remained resistant. Flow cytometric analysis revealed cell cycle perturbations in S-phase only in the DU-145 cells. 5-FdU-NOAC caused 50% inhibition of thymidylate synthase after 90 min at 0.6 microM in both cell lines. Apoptotic cell fractions in DU-145 (66%) and in PC-3 (34%) cells were found after treatment with 5-FdU-NOAC for 96 hr. DNA fragmentation further confirmed the induction of apoptosis.. 5-FdU-NOAC inhibits thymidylate synthase and cell cycle progression causing proliferation arrest and apoptosis in DU-145 and PC-3 cells, suggesting a potential role of 5-FdU-NOAC for the treatment of prostate cancer.

Topics: Androgens; Antimetabolites, Antineoplastic; Apoptosis; Biotransformation; Cell Cycle; Cell Division; Cytarabine; Dimerization; Dose-Response Relationship, Drug; Enzyme Inhibitors; Floxuridine; Fluorodeoxyuridylate; Humans; Hydrolysis; Male; Neoplasms, Hormone-Dependent; Phosphodiesterase I; Phosphoric Diester Hydrolases; Prodrugs; Prostatic Neoplasms; Thymidylate Synthase; Tumor Cells, Cultured; Tumor Suppressor Protein p53

2000