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This study was aimed to observe the expression of P70 S6 kinase(P70 S6K)in oral acinic cell carcinoma.PT0 S6 kinase expression was examined by means of Western-blot test and Activity as- say.Specimens were from 30 cases of oral acinic cell carcinoma and 15 cases of normal oral tissue were used as controls.Statistical analysis software SPSS10.0 was used for t test to determine the relationship between gene expression and clinical features.The expression level of P70 S6K increased obviously in oral acinic cell carcinoma tissue(P<0.01).Activity assay was the same as the Westemblot test(P<0.01).P70 S6K expression level and activity played an important role in the development of oral acinic cell carcinoma.In conclusion,P70 S6K is amplified and overexpressed in oral acinic cell carci- noma tissue,which suggests a potential oncogenic function.P70 S6K and other possible targets of mTOR contribute significantly to tumor development and that inhibition of these proteins may be thera- peutic for cancer patients.Overexpression of P70 S6K may be involved in the pathogenesis of oral acin- ic cell carcinoma.
This study was aimed to observe the expression of P70 S6 kinase (P70 S6K) in oral acinic cell carcinoma. PT0 S6 kinase expression was examined by means of Western-blot test and Activity as- say. Specimens were from 30 cases of oral acinic cell carcinoma and 15 cases of normal oral tissue were used as controls. Statistical analysis software SPSS10.0 was used for t test to determine the relationship between gene expression and clinical features. The expression level of P70 S6K increased obviously in oral acinic cell carcinoma tissue ( P70 S6K expression level and activity played an important role in the development of oral acinic cell carcinoma. In conclusion, P70 S6K was amplified and overexpressed in oral (P <0.01) .Activity assay was the same as the Westemblot test acinic cell carci- noma tissue, which suggests a potential oncogenic function. P70 S6K and other possible targets of mTOR contribute significantly to tumor development and that inhibition of these proteins may be thera- peutic for cancer patients. Overexpression of P70 S6K may be involved in the pathogenesis of oral acin-ic cell carcinoma.