https://scholars.lib.ntu.edu.tw/handle/123456789/544421
Title: | Anthraquinone derivatives induce G2/M cell cycle arrest and apoptosis in NTUB1 cells | Authors: | Tu H.-Y. Huang A.-M. Teng C.-H. Hour T.-C. Yang S.-C. YEONG-SHIAU PU Lin C.-N. |
Keywords: | Anthraquinone; Anticancer; Bax; CyclinB1; p21; p53; Reactive oxygen species; Synthesis | Issue Date: | 2011 | Journal Volume: | 19 | Journal Issue: | 18 | Start page/Pages: | 5670-5678 | Source: | Bioorganic and Medicinal Chemistry | Abstract: | Thirteen anthraquinone derivatives 5-17 including two 3-(3- alkylaminopropoxy)-9,10-anthraquinone (NHA) derivatives 5 and 6, and 11 1-hydroxy-3-(3-alkylaminopropoxy)-9,10-anthraquinone (MHA) derivatives 7-17 were synthesized, evaluated for cytotoxicities against two cancer cell lines, and assayed the generation of reactive oxygen species (ROS) in NTUB1 cells (a human bladder carcinoma cell line). Compound 9 bearing a pyrrolidinyl group induced the stronger cytotoxic effect than those of other synthesized NHA and MHA derivatives. Exposure of NTUB1 cells to 9, 13, and 17 for 24 h significantly increased the production of ROS, respectively. Flow cytometric analysis exhibited that the exposure of NTUB1 cells to the selective 9 led to the G2/M phase arrest accompanied by an increase of apoptotic cell death after the incubation for 24 h. Compound 9 induced up-regulation of cyclinB1 and p21 expressions. Biological results suggested that the induction of G2/M arrest, apoptosis, and cell death by 9 may associate with increased expression of p21 and cyclin B1, elevation of Bax and p53 levels, and generation of ROS in the cell. In conclusion, these series of compounds may be used as anticancer agents. ? 2011 Elsevier Ltd. All rights reserved. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-80052571005&doi=10.1016%2fj.bmc.2011.07.021&partnerID=40&md5=965b0bbc89bf58d67dce0a3f477e2c12 https://scholars.lib.ntu.edu.tw/handle/123456789/544421 |
ISSN: | 0968-0896 | DOI: | 10.1016/j.bmc.2011.07.021 | SDG/Keyword: | 1 hydroxy 3 [3 (2 hydroxypropylamino)propxy] 9,10 anthraquinone; 1 hydroxy 3 [3 (4 methylpiperazin 1 yl)propxy] 9,10 anthraquinone; 1 hydroxy 3 [3 (cyclohexylamino)propxy] 9,10 anthraquinone; 1 hydroxy 3 [3 (ethylamino)propoxyl] 9,10 anthraquinone; 1 hydroxy 3 [3 (morpholin 4 yl)propxy] 9,10 anthraquinone; 1 hydroxy 3 [3 (piperidin 1 yl)propxy] 9,10 anthraquinone; 1 hydroxy 3 [3 (propylamino)propoxyl] 9,10 anthraquinone; 1 hydroxy 3 [3 (pyrrolidin 1 yl)propoxyl] 9,10 anthraquinone; 1 hydroxy 3 [3 [(2 hydroxyethyl)methylamino]propxy] 9,10 anthraquinone; 1 hydroxy 3 [3 [4 (2 hydroxyethyl)piperazin 1 yl]propxy] 9,10 anthraquinone; 3 [3 (dimethylamino)propoxyl] 9,10 anthraquinone; 3 [3 (ethylamino)propoxyl] 9,10 anthraquinone; 4 [3 (4 hydroxy 9,10 dioxo 9,10 dihydro anthracen 2 yloxy)propyl]piperazine 1 carboxylic acid ethyl ester; anthraquinone derivative; cyclin B1; cyclin dependent kinase inhibitor 1; cyclin dependent kinase inhibitor 1B; protein Bax; protein Noxa; protein p53; PUMA protein; unclassified drug; apoptosis; article; cancer cell culture; cell cycle arrest; cell cycle G2 phase; cell cycle M phase; cell cycle progression; cell cycle S phase; cell death; down regulation; drug cytotoxicity; drug screening; drug structure; drug synthesis; drug toxicity; fluorescence activated cell sorting; human; immunofluorescence; quantitative analysis; upregulation; Anthraquinones; Antineoplastic Agents; Apoptosis; Cell Cycle; Cell Division; Cell Line, Tumor; Cell Proliferation; Dose-Response Relationship, Drug; Drug Screening Assays, Antitumor; G2 Phase; Humans; Molecular Structure; Stereoisomerism; Structure-Activity Relationship |
Appears in Collections: | 醫學系 |
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