1/2/2024 0 Comments Julia ioffe nude![]() ![]() Therefore, we investigated the cytotoxic effects of CPT-11 in promyelocytic leukemia HL- 60 cells and in vivo and tumor growth in a leukemia xenograft model. Irinotecan HCl (CPT-11) is an anticancer prodrug, but there is no available information addressing CPT-11-inhibited leukemia cells in in vitro and in vivo studies. All rights reserved.Īntitumor effects with apoptotic death in human promyelocytic leukemia HL- 60 cells and suppression of leukemia xenograft tumor growth by irinotecan HCl.Ĭhen, Yung-Liang Chueh, Fu-Shin Yang, Jai-Sing Hsueh, Shu-Ching Lu, Chi-Cheng Chiang, Jo-Hua Lee, Ching-Sung Lu, Hsu-Feng Chung, Jing-Gung Collectively, gossypol treatment can reduce phosphorylation of Bcl-2 at serine 70 in leukemia HL- 60 cells and gossypol may be a promising therapeutical candidate for leukemia patients especially expressing phosphorylated Bcl-2 at Ser70. In addition, pre-treatment of PDBu partially prevented gossypol-induced apoptosis in HL- 60 cells. This reduction was found to be not only in both dose- and time-dependent fashion but also obviated by phorbol l2,13-dibutyrate (PDBu), an activator of protein kinase C (PKC). However, phosphorylation of Bcl-2 at serine 70 (phospho S70) was strikingly down-regulated in gossypol-exposed cells. ![]() Bcl-2/Bcl-xL/Mcl-1 protein levels were slightly reduced and phosphorylation of Bcl-2 at threonine 56 (phospho T56) was not altered. We found that gossypol treatment inhibited cell growth and induced apoptosis in HL- 60 cells. Here we investigate the alterations of Bcl-2/Bcl-xL/Mcl-1 protein levels and Bcl-2 phosphorylation in gossypol-induced apoptosis in human leukemia HL- 60 cells. However, the molecular mechanisms underlying apoptosis induction by gossypol in malignant cells have not been completely enunciated. Gossypol is an attractive therapeutic anti-tumor agent as an apoptosis inducer and is being evaluated in preclinical tests. Huang, Li-heng Hu, Jia-qi Tao, Wei-qun Li, Yuan-hong Li, Guan-ming Xie, Pei-yi Liu, Xiao-shan Jiang, Jikai Gossypol inhibits phosphorylation of Bcl-2 in human leukemia HL- 60 cells. These data suggest that morphinone induces non-apoptotic cell death in HL- 60 cells. The autophagy inhibitor 3-methyladenine (0.3-10 mM) slightly inhibited the morphinone-induced cytotoxicity, when corrected for its own cytotoxicity. Electron microscopy demonstrated that morphinone induced mitochondrial shrinkage, vacuolization and production of autophagosome and the loss of cell surface microvilli, without destruction of cell surface and nuclear membranes in the HL- 60 cells. ![]() Morphinone dose-dependently activated caspase-3 in both HL- 60 and HSC-2 cell lines, but to a much lesser extent than actinomycin D. Morphinone did not activate caspase-8 or -9 in these cells. Morphinone also induced an almost undetectable level of internucleosomal DNA fragmentation in the HL- 60 cells. Morphinone showed slightly higher cytotoxic activity against human tumor cell lines (oral squamous cell carcinoma HSC-2, HSC-3, HSC-4, NA, Ca9-22, promyelocytic leukemia HL- 60, cervical carcinoma HeLa) than against normal oral human cells (gingival fibroblast HGF, pulp cells HPC, periodontal ligament fibroblast HPLF). Whether, morphinone, an oxidative metabolite of morphine, also induced a similar type of cell death in HL- 60 cells was investigated. Takeuchi, Risa Hoshijima, Hiroshi Nagasaka, Hiroshi Chowdhury, Shahead Ali Kikuchi, Hirotaka Kanda, Yumiko Kunii, Shiro Kawase, Masami Sakagami, HiroshiĪs previously suggested, codeinone (oxidation product of codeine) induces non-apoptotic cell death, characterized by marginal caspase activation and the lack of DNA fragmentation in HL- 60 human promyelocytic leukemia cells, which was inhibited by N-acetyl-L-cysteine. Induction of non-apoptotic cell death by morphinone in human promyelocytic leukemia HL- 60 cells. ![]()
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