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Inhibitory effects of CP on the growth of human gastric adenocarcinoma BGC-823 tumours in nude mice

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机构: [1]Hebei Med Univ, Affiliated Hosp 2, Dept Surg, Shijiazhuang, Hebei, Peoples R China [2]Hebei Med Univ, Tradit Chinese Med Coll, Dept Biochem & Mol Biol, Hebei Key Lab Chinese Med Res Cardiocerebrovasc D, Shijiazhuang, Hebei, Peoples R China [3]Qinhuangdao Hlth Sch, Dept Clin Med, Qinhuangdao, Hebei, Peoples R China [4]Department of Surgery, Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei Province, China
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关键词: CP gastric carcinoma BGC-823 cells proliferation apoptosis

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Objective To investigate the potential antitumour effects of [2-(6-amino-purine-9-yl)-1-hydroxy-phosphine acyl ethyl] phosphonic acid (CP) against gastric adenocarcinoma. Methods Human BGC-823 xenotransplants were established in nude mice. Animals were randomly divided into control and CP groups, which were administered NaHCO3 vehicle alone or CP dissolved in NaHCO3 (200 mu g/kg body weight) daily, respectively. Tumour volume was measured weekly for 6 weeks. Resected tumours were assayed for proliferative activity with anti-Ki-67 or anti-proliferating cell nuclear antigen (PCNA) antibodies. Cell apoptosis was examined using terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) assays and with caspase-3 immunostaining. Proteins were measured by Western blotting. Results There was a significant reduction in tumour volume and a reduced percentage of Ki-67-positive or PCNA-positive cells in the CP group compared with the control group. The percentage of TUNEL-positive or caspase 3-positive cells significantly increased following CP treatment compared with the control group. Tumours from the CP group had higher levels of phosphorylated-extracellular signal-regulated kinase (p-ERK) and phosphorylated-AKT (p-AKT) compared with control tumours. Conclusion CP treatment inhibited tumour growth and induced tumour cell apoptosis in a nude mouse model of BGC-823 gastric adenocarcinoma. Activation of the AKT and ERK signalling pathways may mediate this antitumour activity.

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出版当年[2018]版:
大类 | 4 区 医学
小类 | 4 区 医学:研究与实验 4 区 药学
最新[2025]版:
大类 | 4 区 医学
小类 | 4 区 医学:研究与实验 4 区 药学
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出版当年[2018]版:
Q4 PHARMACOLOGY & PHARMACY Q4 MEDICINE, RESEARCH & EXPERIMENTAL
最新[2023]版:
Q4 MEDICINE, RESEARCH & EXPERIMENTAL Q4 PHARMACOLOGY & PHARMACY

影响因子: 最新[2023版] 最新五年平均 出版当年[2018版] 出版当年五年平均 出版前一年[2017版] 出版后一年[2019版]

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第一作者机构: [1]Hebei Med Univ, Affiliated Hosp 2, Dept Surg, Shijiazhuang, Hebei, Peoples R China
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通讯机构: [4]Department of Surgery, Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei Province, China [*1]Department of Surgery, Fourth Affiliated Hospital of Hebei Medical University, 12 Jiankang Road, Shijiazhuang 050011, Hebei Province, China
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