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1.
Zhongguo Zhong Yao Za Zhi ; 44(1): 119-124, 2019 Jan.
Artigo em Chinês | MEDLINE | ID: mdl-30868822

RESUMO

To explore the mechanism of ß-carboline alkaloids inhibiting the migration and invasion of SGC-7901 cells and its correlation with FAK gene expression,CCK-8 method was used to determine the inhibitory rate of ß-carboline alkaloids on the proliferation of gastric cancer SGC-7901 cells under different concentrations.The effect of ß-carboline alkaloids on the migration and invasion of SGC-7901 cells was used by Transwell compartment.Detection of mRNA and protein expression of FAK genes were used by qRT-PCR and Western blot.Then si-FAK-1051 recombinant plasmid was transfected into SGC-7901 cells.FAK gene silencing effect was identified by qRT-PCR and Western blot technique again.Finally,the effects of FAK gene silencing on proliferation and migration of gastric cancer SGC-7901 cells were detected by CCK-8 kit and Transwell chamber assay respectively.With the increase of the concentration ofß-carboline alkaloids,the inhibitory rate of SGC-7901 cells in human gastric cancer cells increased gradually,with IC5013.364 mg·L-1.The number of SGC-7901 cells of Transwell compartment in the positive experimental group(5-FU,5 mg·L-1) and the ß-carboline alkaloids group decreased significantly(P<0.01) and the number of SGC-7901 cells in the ß-carboline alkaloids group was significantly lower than that in the positive experimental group(P<0.01).Compared with the blank control group,the mRNA and protein expression level of FAK genes in the positive experimental group was significantly lower than that in the experimental group of ß-carboline alkaloids(P<0.05).After transfection of si-FAK-1051 into gastric cancer SGC-7901 cells,the expression of mRNA and protein of FAK gene was significantly down regulated(P<0.05).SGC-7901 cell proliferation and cell migration ability also decreased significantly(P<0.05).ß-carboline alkaloids are more effective than 5-FU in inhibiting migration and invasion of gastric cancer SGC-7901 cells,and the mechanism may be related to the inhibition of mRNA and protein expression of FAK gene by ß-carboline alkaloids.


Assuntos
Alcaloides/farmacologia , Carbolinas/farmacologia , Movimento Celular/efeitos dos fármacos , Invasividade Neoplásica , Neoplasias Gástricas/patologia , Linhagem Celular Tumoral , Proliferação de Células , Quinase 1 de Adesão Focal/genética , Regulação Neoplásica da Expressão Gênica , Inativação Gênica , Humanos , Neoplasias Gástricas/tratamento farmacológico
2.
Diagn Pathol ; 8: 33, 2013 Feb 22.
Artigo em Inglês | MEDLINE | ID: mdl-23432846

RESUMO

BACKGROUND: The determination of sensitive chemotherapy drugs for gastric cancer (GC) is one of the greatest challenges of adjuvant therapy. Here we evaluated the chemosensitivity of GC to anticancer drugs and the telomerase reverse transcriptase (hTERT) mRNA expression, and investigated the relationship of them. METHODS: The GC cells which were collected from 68 patients with primary GC were primary cultured. The chemosensitivity of GC cells to anticancer drugs was evaluated successfully using the MTT assay for 60 cases of GC cells, and the hTERT mRNA expression was examined in 60 cases of GC tissues and corresponding normal gastric mucosa and 6 cases of chronic superficial gastritis mucosa by in situ hybridization. RESULTS: Taxol, cisplatin and 5-fluorouracil were in general more effective than adriamycin and mitomycin for GC cells, and the chemosensitivity to anticancer drugs was associated with tumor histological types and a worse tumor grade. Compared to normal gastric mucosa tissues, hTERT mRNA expression was significantly increased in GC (P<0.05), which was related with a worse differentiation and drug-resistance to 5-fluorouracil or adriamycin in GC. CONCLUSIONS: These data demonstrate for the first time that examinations of hTERT mRNA expression as an important factor could be used to select the chemotherapeutic drugs for GC patients. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1793217009875483.


Assuntos
Adenocarcinoma/genética , Antineoplásicos/farmacologia , Biomarcadores Tumorais/genética , Resistencia a Medicamentos Antineoplásicos/genética , RNA Mensageiro/metabolismo , Neoplasias Gástricas/genética , Telomerase/genética , Adenocarcinoma/enzimologia , Adenocarcinoma/patologia , Adenocarcinoma Mucinoso/enzimologia , Adenocarcinoma Mucinoso/genética , Adenocarcinoma Mucinoso/patologia , Adenocarcinoma Papilar/enzimologia , Adenocarcinoma Papilar/genética , Adenocarcinoma Papilar/patologia , Carcinoma de Células em Anel de Sinete/enzimologia , Carcinoma de Células em Anel de Sinete/genética , Carcinoma de Células em Anel de Sinete/patologia , Estudos de Casos e Controles , Diferenciação Celular , Sobrevivência Celular/efeitos dos fármacos , Cisplatino/farmacologia , Doxorrubicina/farmacologia , Ensaios de Seleção de Medicamentos Antitumorais , Fluoruracila/farmacologia , Regulação Enzimológica da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Humanos , Hibridização In Situ , Mitomicina/farmacologia , Gradação de Tumores , Paclitaxel/farmacologia , Neoplasias Gástricas/enzimologia , Neoplasias Gástricas/patologia , Células Tumorais Cultivadas
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