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1.
Zhonghua Yi Xue Za Zhi ; 96(32): 2545-7, 2016 Aug 23.
Artigo em Chinês | MEDLINE | ID: mdl-27596548

RESUMO

OBJECTIVE: To analyze the correlation between glycolipids metabolism and clinicopathologic features in patients with gastric cancer. METHODS: Glycolipids metabolism and clinicopathologic features of 443 gastric cancer patients were collected, and their correlation was analyzed. RESULTS: Compared to gastric cancer patients with normal levels of glycolipids metabolism, there were less male patients who were with low level of total cholesterol (TCH)(χ(2)=7.676, P<0.05), and the number of male patients with low level of high-density lipoprotein (HDL) (χ(2)=7.520) and apoA1 (χ(2)=6.253) was higher (both P<0.05). Serum TCH level showed a negative correlation with age of patients (r=-0.116), tumor size (r=-0.117) and TNM stage (r=-0.111) (P<0.05); serum HDL level was negatively correlated with tumor diameter (r=-0.094), the number of metastatic lymph nodes (r=-0.106), primary tumor invasion depth (r=-0.112), metastatic lymph nodes stage (r=-0.102) and TNM stage (r=-0.107) (P<0.05); serum LDL was negatively correlated with age of patients (r=-0.116) (P<0.05); serum LPa was positively correlated with tumor size (r=0.170), the number of metastatic lymph nodes (r=0.151), primary tumor invasion depth (r=0.160), metastatic lymph nodes stage (r=0.153) and TNM stage (r=0.115) (P<0.05); apoA1 was negatively correlated with distant metastasis (r=-0.168) and TNM stage (r=-0.120) (P<0.05); and apoB was negatively correlated with distant metastases (r=-0.132, P<0.05). Levels of blood glucose and TG had no significant association with clinicopathological features of gastric cancer patients (P>0.05). CONCLUSIONS: Low lipid metabolism but high level of LPa may be the metabolic characteristics of gastric cancer progression. Monitoring the changes of serum lipids levels could be valuable for the prognosis of patients with gastric cancer.


Assuntos
Metabolismo dos Lipídeos , Neoplasias Gástricas , Glicolipídeos , Humanos , Linfonodos , Masculino , Prognóstico
2.
Eur Rev Med Pharmacol Sci ; 20(7): 1244-50, 2016 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-27097942

RESUMO

OBJECTIVE: N1-guanyl-1, 7-diaminoheptane (GC7), an inhibitor of deoxyhypusine synthase has been shown to exhibit significant anti-cancer activity. However, the biological role of eukaryotic translation initiation factor 5A2 activation (EIF5A2) and GC7 on drug resistance in non-small cell lung cancer (NSCLC) has not been investigated. In this study, we aimed to investigate the therapeutic effect of GC7 combined with cetuximab in NSCLC therapy. MATERIALS AND METHODS: The current study used cell viability assays, EdU incorporation assays, and western blot to detect that the GC7 exhibited synergistic cytotoxicity with cetuximab in NSCLC. RESULTS: CCK-8 assays showed that combined treatment with GC7 and cetuximab significantly inhibited the viabilities in three NSCLC cell lines. In addition, EdU incorporation assays also indicated that GC7 co-treatment remarkably enhanced the cetuximab sensitivity in NSCLC cells. Nevertheless, down-regulation of EIF5A2 diminished the regulatory role of GC7 in cetuximab cytotoxicity. Western blot showed that transfection of EIF5A2 siRNA significantly suppressed the protein expression of EIF5A2 in NSCLC cells. CONCLUSIONS: These findings demonstrate that combined treatment with GC7 could enhance cetuximab sensitivity by inhibiting EIF5A2 in NSCLC cells, implying the potential clinical application of GC7 in cetuximab-based chemotherapy for NSCLC patients.


Assuntos
Carcinoma Pulmonar de Células não Pequenas/patologia , Cetuximab/farmacologia , Guanina/análogos & derivados , Neoplasias Pulmonares/patologia , Fatores de Iniciação de Peptídeos/genética , Proteínas de Ligação a RNA/genética , Carcinoma Pulmonar de Células não Pequenas/genética , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/genética , Regulação para Baixo/efeitos dos fármacos , Regulação para Baixo/genética , Resistencia a Medicamentos Antineoplásicos/efeitos dos fármacos , Resistencia a Medicamentos Antineoplásicos/genética , Sinergismo Farmacológico , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Guanina/farmacologia , Humanos , Neoplasias Pulmonares/genética , Fatores de Iniciação de Peptídeos/metabolismo , RNA Interferente Pequeno/farmacologia , Proteínas de Ligação a RNA/metabolismo , Fator de Iniciação de Tradução Eucariótico 5A
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