2018Zhonghua shiyan waike zazhiRequires access

Tumor growth in bearing PC-9 mice on treatment of tumor necrosis factor-related apoptosis-inducing ligand combined with cisplatin and anti-tumor mechanism analysis

Chunyang Zhang, Yu Qi, Kai Wu, Yan Zhang

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Abstract

Objective To explore Tumor growth in bearing PC-9 mice on treatment of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) combined with cisplatin and anti-tumor mechanism analysis. Methods Sixty nude mice bearing human lung adenocarcinoma PC-9 xenografted tumor were randomly divided into Control group, TRAIL group, cisplatin group and combination group. Mice in TRAIL group were treated with TRAIL (10 mg/kg) by intraperitoneal injection. Mice in cisplatin group were treated with cisplatin (1.5 mg/kg) by intraperitoneal injection. Mice in combination group were treated with TRAIL (10 mg/kg) and cisplatin (1.5 mg/kg) by intraperitoneal injection. Mice in control group were treated with phosphate buffer (PBS) by intraperitoneal injection. After 30 days of treatment, tumor growth, survival and body weight among four groups were analyzed. Apotosis of tumor cell in four groups were analyzed by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. Apotosis proteins p53 and Caspase-3 were analyzed by Western blotting. Results Compared with the control group, tumor growth in TRAIL group, cisplatin group and combination group were significantly inhibited (P=0.030, 0.026, 0.009), while tumor growth rate in combination group was significantly slower than that of TRAIL group and cisplatin group (P=0.036, 0.018). Compared with the control group, the body weight of the cisplatin group and the combined treatment group was significantly decreased (P=0.030, 0.038), while there was no difference in body weight change (P=0.070) between TRAIL group and control group. Compared with control group, the proportion of apoptosis in TRAIL group, cisplatin group and combination group was significantly increased(P=0.023, 0.034, 0.027). Compared with the cisplatin group, the apoptosis ratio of TRAIL group and combination group was significantly increased(P=0.028, 0.013). Compared with control group, the expression of p53 and Caspase-3 in the TRAIL group, cisplatin group and combined treatment group were significantly increased, while the increase in the combined treatment group was more significant (P=0.018). Conclusion Tumor necrosis factor related apoptosis inducing ligand (TRAIL) combined with cisplatin can significantly inhibit the growth of PC-9 tumor bearing mice, this phenomenon is by promoting tumor cell apoptosis related gene expression and promote apoptosis of tumor cells and the. Key words: Tumor necrosis factor related apoptosis inducing ligand; Cisplatin; Apoptosis; Tumor growth

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Objective To explore Tumor growth in bearing PC-9 mice on treatment of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) combined with cisplatin and anti-tumor mechanism analysis. Methods Sixty nude mice bearing human lung adenocarcinoma PC-9 xenografted tumor were randomly divided into Control group, TRAIL group, cisplatin group and combination group. Mice in TRAIL group were treated with TRAIL (10 mg/kg) by intraperitoneal injection. Mice in cisplatin group were treated with cisplatin (1.5 mg/kg) by intraperitoneal injection. Mice in combination group were treated with TRAIL (10 mg/kg) and cisplatin (1.5 mg/kg) by intraperitoneal injection. Mice in control group were treated with phosphate buffer (PBS) by intraperitoneal injection. After 30 days of treatment, tumor growth, survival and body weight among four groups were analyzed. Apotosis of tumor cell in four groups were analyzed by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. Apotosis proteins p53 and Caspase-3 were analyzed by Western blotting. Results Compared with the control group, tumor growth in TRAIL group, cisplatin group and combination group were significantly inhibited (P=0.030, 0.026, 0.009), while tumor growth rate in combination group was significantly slower than that of TRAIL group and cisplatin group (P=0.036, 0.018). Compared with the control group, the body weight of the cisplatin group and the combined treatment group was significantly decreased (P=0.030, 0.038), while there was no difference in body weight change (P=0.070) between TRAIL group and control group. Compared with control group, the proportion of apoptosis in TRAIL group, cisplatin group and combination group was significantly increased(P=0.023, 0.034, 0.027). Compared with the cisplatin group, the apoptosis ratio of TRAIL group and combination group was significantly increased(P=0.028, 0.013). Compared with control group, the expression of p53 and Caspase-3 in the TRAIL group, cisplatin group and combined treatment group were significantly increased, while the increase in the combined treatment group was more significant (P=0.018). Conclusion Tumor necrosis factor related apoptosis inducing ligand (TRAIL) combined with cisplatin can significantly inhibit the growth of PC-9 tumor bearing mice, this phenomenon is by promoting tumor cell apoptosis related gene expression and promote apoptosis of tumor cells and the. Key words: Tumor necrosis factor related apoptosis inducing ligand; Cisplatin; Apoptosis; Tumor growth

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Available abstract

Objective To explore Tumor growth in bearing PC-9 mice on treatment of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) combined with cisplatin and anti-tumor mechanism analysis. Methods Sixty nude mice bearing human lung adenocarcinoma PC-9 xenografted tumor were randomly divided into Control group, TRAIL group, cisplatin group and combination group. Mice in TRAIL group were treated with TRAIL (10 mg/kg) by intraperitoneal injection. Mice in cisplatin group were treated with cisplatin (1.5 mg/kg) by intraperitoneal injection. Mice in combination group were treated with TRAIL (10 mg/kg) and cisplatin (1.5 mg/kg) by intraperitoneal injection. Mice in control group were treated with phosphate buffer (PBS) by intraperitoneal injection. After 30 days of treatment, tumor growth, survival and body weight among four groups were analyzed. Apotosis of tumor cell in four groups were analyzed by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. Apotosis proteins p53 and Caspase-3 were analyzed by Western blotting. Results Compared with the control group, tumor growth in TRAIL group, cisplatin group and combination group were significantly inhibited (P=0.030, 0.026, 0.009), while tumor growth rate in combination group was significantly slower than that of TRAIL group and cisplatin group (P=0.036, 0.018). Compared with the control group, the body weight of the cisplatin group and the combined treatment group was significantly decreased (P=0.030, 0.038), while there was no difference in body weight change (P=0.070) between TRAIL group and control group. Compared with control group, the proportion of apoptosis in TRAIL group, cisplatin group and combination group was significantly increased(P=0.023, 0.034, 0.027). Compared with the cisplatin group, the apoptosis ratio of TRAIL group and combination group was significantly increased(P=0.028, 0.013). Compared with control group, the expression of p53 and Caspase-3 in the TRAIL group, cisplatin group and combined treatment group were significantly increased, while the increase in the combined treatment group was more significant (P=0.018). Conclusion Tumor necrosis factor related apoptosis inducing ligand (TRAIL) combined with cisplatin can significantly inhibit the growth of PC-9 tumor bearing mice, this phenomenon is by promoting tumor cell apoptosis related gene expression and promote apoptosis of tumor cells and the. Key words: Tumor necrosis factor related apoptosis inducing ligand; Cisplatin; Apoptosis; Tumor growth

Key concepts: Cisplatin, Apoptosis, Intraperitoneal injection, TUNEL assay, Tumor necrosis factor alpha, Necrosis, Endocrinology, Chemistry

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Tumor growth in bearing PC-9 mice on treatment of tumor necrosis factor-related apoptosis-inducing ligand combined with cisplatin and anti-tumor mechanism analysis — Research Paper | ScholarLens