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Dis Esophagus ; 30(7): 1-7, 2017 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-30052898

RESUMO

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.


Assuntos
Antimetabólitos Antineoplásicos/farmacologia , Carcinoma de Células Escamosas/terapia , Neoplasias Esofágicas/terapia , Fluoruracila/farmacologia , Expressão Gênica , Hipertermia Induzida , Subfamília B de Transportador de Cassetes de Ligação de ATP/genética , Apoptose/efeitos dos fármacos , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Terapia Combinada , Di-Hidrouracila Desidrogenase (NADP)/genética , Expressão Gênica/efeitos dos fármacos , Humanos , Orotato Fosforribosiltransferase/genética , RNA Mensageiro/metabolismo , Timidilato Sintase/genética , Proteína Supressora de Tumor p53/genética , Proteína X Associada a bcl-2/genética
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