RESUMEN
The abnormality of serine/threonine kinase Aurora-A is seen in many types of cancers. Although in physiological context it has been shown to play a vital role in cellular mitosis, how this oncogene contributes to tumorigenesis remains unclear. Here we demonstrate that Aurora-A overexpression enhances both the expression level and transcriptional activity of c-Myc. The inhibition of c-Myc expression by RNA interference significantly impaired the oncogenic potential of Aurora-A, resulting in attenuated cellular proliferation and transformation rates as well as fewer centrosomal aberrations. Furthermore, downregulation of c-Myc effectively overcame Aurora-A-induced resistance to cisplatin in esophageal cancer cells. Taken together, our results suggest an important role for c-Myc in mediating the oncogenic activity of Aurora-A, which may in turn allow for future targeting of c-Myc as a potential therapeutic strategy for tumors with Aurora-A overexpression.
Asunto(s)
Humanos , Línea Celular Transformada , Proliferación Celular/efectos de los fármacos , Transformación Celular Neoplásica/efectos de los fármacos , Cisplatino/farmacología , Regulación hacia Abajo , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Proteínas Serina-Treonina Quinasas/genética , Proteínas Proto-Oncogénicas c-myc/genética , ARN Interferente Pequeño/genética , Activación Transcripcional , Transgenes/genéticaRESUMEN
Chloroporphyrin derivative (CPD1) 20mg ? L-1 plus light 5min caused marked photohemolyses, At the dose of 10mg ? L-1 20mg ? L-1 plus light10min. the activities of AchEs in red cell membane and ATPase in liver mitochondria and G-6-Plus in liver microsome were markedly inhibited lipid peroxida- tion of red cell membrane was greatly enhanced by CPD1 plus light when CPD1 was irrad - iated the production of free radical of superoxide anion was initiated the amount of O2 production was depen-dent on CPD1 doses and irradiation time.