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Dis Esophagus ; 30(7): 1-7, 2017 Jul 01.
Artículo en Inglés | MEDLINE | ID: mdl-30052898

RESUMEN

Esophageal squamous cell carcinoma is a highly aggressive neoplasm and the sixth leading cause of global cancer-related death; the 5-year survival rate for esophageal cancer is only about 20%-25% for all stages. Therefore, improving the therapeutic effect is important. This study assessed whether low-dose hyperthermia (LDH) enhances the antitumor effects of chemotherapy. The antitumor effect of chemotherapy with/without LDH in the squamous cell carcinoma cell line SCCVII was evaluated. A comprehensive analysis was performed with real-time polymerase chain reaction (PCR) to study the hyperthermia-induced changes in the gene expression of SCCVII cell lines. In addition, the cytotoxic and apoptotic changes in the cells treated with LDH combined with/without 5-fluorouracil (5-FU) were measured. LDH combined with 5-FU (10 nM) strongly inhibited the cell growth of SCCVII, with flow cytometry showing an increased population of apoptotic cells. PCR showed that LDH promoted a 25.22-fold increase of p53 mRNA and 18.08-fold increase of Bax mRNA in vitro. MDR1 expression was decreased to 28.7% after LDH. This treatment can result in much higher efficacy of antitumor drugs. After LDH, the expressions of TS decreased to 12.06%, OPRT increased by 4.17-fold, and DPD did not change (1.03-fold). This transformations will induce susceptibility to 5-FU. LDH may be a useful enhancer of chemotherapy drugs for squamous cell carcinoma.


Asunto(s)
Antimetabolitos Antineoplásicos/farmacología , Carcinoma de Células Escamosas/terapia , Neoplasias Esofágicas/terapia , Fluorouracilo/farmacología , Expresión Génica , Hipertermia Inducida , Subfamilia B de Transportador de Casetes de Unión a ATP/genética , Apoptosis/efectos de los fármacos , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Terapia Combinada , Dihidrouracilo Deshidrogenasa (NADP)/genética , Expresión Génica/efectos de los fármacos , Humanos , Orotato Fosforribosiltransferasa/genética , ARN Mensajero/metabolismo , Timidilato Sintasa/genética , Proteína p53 Supresora de Tumor/genética , Proteína X Asociada a bcl-2/genética
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