RESUMO
This study was designed to investigate the effect of digoxin on migration and invasion of human gastric carcinoma MKN45 cells and its possible mechanism. MKN45 cells were treated with different concentrations of digoxin for 24 h. The shRNA-AEG-1 plasmid was transfected into MKN45 cells via lipofectamine to block the expression of astrocyte elevated gene-1 (AEG-1). Western blot was used to analyze the protein levels of matrix metalloproteinase-9 (MMP-9), E-cadherin and AEG-1. The result showed that digoxin reduced the abilities of migration and invasion (P < 0.05), up-regulated the protein level of E-cadherin (P < 0.05), and down-regulated the protein levels of MMP-9 and AEG-1 (P < 0.05) in MKN45 cells in a dose-dependent manner. Compared with shControl group, shAGE-1 group showed inhibited cellular migration and invasion, higher expression level of E-cadherin, and lower expression levels of MMP-9 and AEG-1. These results suggest that digoxin suppresses the migration and invasion of human gastric carcinoma MKN45 cells in a dose-dependent manner through inhibiting the expression of AEG-1, and then resulting in the up-regulation of the protein expression of E-cadherin and the down-regulation of the protein expression of MMP-9.
Assuntos
Moléculas de Adesão Celular/metabolismo , Movimento Celular/efeitos dos fármacos , Digoxina/farmacologia , Regulação Neoplásica da Expressão Gênica , Neoplasias Gástricas/patologia , Antígenos CD , Caderinas/metabolismo , Linhagem Celular Tumoral , Regulação para Baixo , Humanos , Metaloproteinase 9 da Matriz/metabolismo , Proteínas de Membrana , Invasividade Neoplásica , RNA Interferente Pequeno/metabolismo , Proteínas de Ligação a RNA , Transfecção , Regulação para CimaRESUMO
The aim of this study was to investigate the effects of AEG-1 gene silencing on the chemoresistance of human breast cancer cell line MCF-7/ADM and its possible mechanism. MCF-7/ADM cells were incubated in the medium containing adriamycin (ADM). The recombinant pLKO.1-shAEG-1 plasmid was constructed to silence AEG-1 expression in human breast cancer MCF-7/ADM cells. MTT assay was employed to detect the anti-tumor effect of ADM on MCF-7/ADM cells, and IC50 value of ADM was calculated according to MTT. Flow cytometry was used to determine the apoptosis. Western blot was used to analyze the expression levels of AEG-1, p-Akt, p-MDM2, p-Bad, p53 and MDR1. The result showed MCF-7/ADM had a significantly higher expression level of AEG-1 compared with that of MCF-7 (P < 0.05), however, the expression of AEG-1 was decreased after AEG-1 gene silencing. The IC50 value of ADM in shAEG-1 group was significantly lower than that in shcontrol group. AEG-1 gene silencing induced cell apoptosis and enhanced the pro-apoptotic effect of ADM on MCF-7/ADM cells. After AEG-1 gene silencing, the phosphorylation of Akt, MDM2 and Bad was inhibited (P < 0.05), the protein levels of p53 and MDR1 were up-regulated (P < 0.05) and down-regulated (P < 0.05) respectively, compared with control. In conclusion, the results suggest that AEG-1 gene silencing can reverse the ADM resistance in human breast cancer cell line MCF-7/ADM by means of inducing apoptosis and down-regulating the protein level of MDR1.
Assuntos
Moléculas de Adesão Celular/genética , Doxorrubicina/farmacologia , Resistencia a Medicamentos Antineoplásicos/genética , Inativação Gênica , Apoptose , Neoplasias da Mama/genética , Neoplasias da Mama/metabolismo , Moléculas de Adesão Celular/metabolismo , Humanos , Células MCF-7 , Proteínas de Membrana , Proteínas de Ligação a RNARESUMO
OBJECTIVE: To investigate the prevalence of human papillomavirus (HPV), particularly of high-risk HPV in biopsy tissue specimens of esophageal carcinomas in Linzhou city. METHODS: General nested primer sets were used to detected the whole HPV genotypes, following by HPV16 and 18 type specific PCR for the HPV16 and 18 detection respectively. RESULTS: All 18 biopsy samples were HPV positive, and HPV 16 was detected in 13 of the 18 samples, HPV 18 was detected in 4 of the 18 samples. CONCLUSION: The high rate of HPV in the esophageal carcinoma samples suggested that HPV infection may be an important etiologic factor in the development of esophageal cancer in Linzhou city.
Assuntos
Neoplasias Esofágicas/virologia , Papillomavirus Humano 16/isolamento & purificação , Papillomavirus Humano 18/isolamento & purificação , Papillomaviridae , Adulto , Idoso , Biópsia , China , Neoplasias Esofágicas/etiologia , Esôfago/patologia , Esôfago/virologia , Feminino , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Papillomaviridae/genética , Reação em Cadeia da PolimeraseRESUMO
OBJECTIVE: To observe therapeutic effect of drug-separated moxibustion at Shenque (CV 8) for treatment of infantile autumn diarrhea. METHODS: One hundred and thirty-six cases were randomly divided into an obser vation group and a control group, 68 cases in each group. The observation group were treated with drug-separated moxibustion at Shenque (CV 8) and the control group with oral administration of Smecta. The mean diarrhea-stopping time, the negative conversion rate of Human Rotavirus antigen in stool after treatment for 72 h, and the markedly-effective rate and the total effective rate were observed after treatment for 6 days in the twO groups. RESULTS: The markedly-effective rate and the total effective rate were 79.4% and 94.1% in the observation group and 35.3% and 75.0% in the control group, respectively, with very significantly or significantly difference between the two groups (P < 0.01 or P < 0.05); the mean diarrhea-stopping time in the observation group was shorter than that in the control group (P < 0.01); the negative conversion rate of Human Rotavirus antigen in stool after treatment for 72 h was 88.2%0 in the observation group and 69.1% in the control group with a very significantly difference between the two groups (P < 0.01). CONCLUSION: Drug-separated moxibustion at Shenque (CV 8) has a significant therapeutic effect on infantile autumn diarrhea, helps negative conversion of Human Rotavirus antigen in stool and shortens duration of disease.