RESUMO
The invasive growth, proliferation, and transcriptional regulation of glioma C6 cells treated with endothelin-1 and PD98059, a specific inhibitor of ERK1/2 were studied. The proliferation of glioma C6 cells was assessed in different growth conditions by prior in vitro treatment with endothelin-1 followed by implantation into the brain. In vitro studies showed that PD98059 inhibited the proliferation of cultured glioma C6 cells and activated transcription factors E2F1 and Myc-Max. Endothelin-1 significantly increased the proliferation of glioma C6 cells. The model used in this study was experimental and may allow the specific features of the in vitro behavior of cultured invasive cells to be identified.
Assuntos
Neoplasias Encefálicas/metabolismo , Neoplasias Encefálicas/patologia , Endotelina-1/farmacologia , Flavonoides/farmacologia , Glioblastoma/metabolismo , Glioblastoma/patologia , Animais , Fatores de Transcrição de Zíper de Leucina Básica/metabolismo , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Células Cultivadas , Fator de Transcrição E2F1/metabolismo , Quinases de Proteína Quinase Ativadas por Mitógeno/antagonistas & inibidores , Invasividade Neoplásica/prevenção & controle , Transplante de Neoplasias , Proteínas Proto-Oncogênicas c-myc/metabolismo , Ratos , Ratos WistarRESUMO
The authors have monitored C6 glioma cell invasive growth, proliferation and transcriptional regulation after pretreatment with endothelin-1 and ERK1/2 specific inhibitor PD98059. To explore proliferation of C6 glioma cells in different growth conditions, they were treated in vitro with endothelin-1 and implanted into the brain. In vitro studies have indicated that PD98059 inhibited the proliferation of cultured C6 glioma cells and induced the activation of E2F1 and Myc-Max transcriptional factors. Endothelin-1 strongly increased C6 glioma cell proliferation. The model used in this study is experimental, but it may provide an insight into the specific behavior of in vitro cultured invasive cells.
