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Tumour Biol ; 36(9): 7121-31, 2015 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-25877754

RESUMO

Newcastle disease virus (NDV), an avian paramyxovirus, possesses the ability to kill tumor cells. Here, we report the effects of NDV strain D90, which was isolated in China, against oral squamous cell carcinoma (OSCC) cells. In this study, we showed that the cell death induced by D90 was apoptotic. Furthermore, the apoptosis induced by D90 was dependent on the mitochondrial pathway, and the death receptor pathway may be not involved. Bax and Bcl-2 also played a role in the apoptosis induced by D90. Lymph node metastasis is a serious problem for oral cancer; we therefore evaluated the impact of D90 on the migration and invasion of OSCC cells. NDV D90 affected microtubules and microfilaments to inhibit the motility of OSCC prior to apoptosis. The effects of D90 on the migration and invasion rates of OSCC cells were evaluated by migration and invasion assays. Subsequently, the changes in sp1, RECK, MMP-2, and MMP-9 induced by a low concentration of D90 were detected by western blot and gelatin zymography. D90 significantly inhibited the invasion and metastasis of OSCC cells by decreasing the expression of sp1 and increasing the expression of RECK to suppress the expression and activity of MMP-2 and MMP-9.


Assuntos
Carcinoma de Células Escamosas/terapia , Proteínas Ligadas por GPI/biossíntese , Metaloproteinase 2 da Matriz/biossíntese , Metaloproteinase 9 da Matriz/biossíntese , Neoplasias Bucais/terapia , Vírus da Doença de Newcastle/genética , Animais , Apoptose/genética , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/patologia , Linhagem Celular Tumoral , Movimento Celular/genética , Proteínas Ligadas por GPI/genética , Humanos , Metástase Linfática , Metaloproteinase 2 da Matriz/genética , Metaloproteinase 9 da Matriz/genética , Mitocôndrias/genética , Mitocôndrias/metabolismo , Neoplasias Bucais/genética , Neoplasias Bucais/patologia , Invasividade Neoplásica/genética , Invasividade Neoplásica/patologia , Terapia Viral Oncolítica , Fator de Transcrição Sp1/biossíntese
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