The activity and the clinical significance of PTEN/PI3K/AKT signalling pathway in clear-cell renal-cell carcinoma
Wei Wang, Hanxin Wu, Jie Zhu, Axiang Xu, Suxia Yang, Xu Zhang
Abstract
Wei Wang, Hanxin Wu, Jie Zhu, Axiang Xu, Suxia Yang, Xu Zhang
Abstract
Objective To discuss the activity of the phosphatase and tensin homologue deleted on chromosome 10 (PTEN)/phosphatidylinositol 3-kinase (PI3K)/AKT pathway and the clinical significance of PTEN protein expression in clear-cell renal-cell carcinoma( CCRCC) tissues. Methods The protein of PTEN and AKT( phosphorylation at Ser473) of 36 paired CCRCC and adjacent non-neoplastic renal samples were analysed by Western blotting. Results The significantly increased AKT (phosphorylation at Ser473 ) with decreased PTEN protein were observed in CCRCC tissues compared with the adjacent non-neoplastic renal samples while the PTEN protein expression has no significant association with pathological parameters. Conclusion Our findings indicated that as PTEN dominantly inhibits AKT activation, the coexistence of high levels of the PTEN protein with enhanced AKT activation suggests the existence of novel mechanisms which attenuate PTEN function in CCRCC. These mechanisms may reduce PTEN function or increase AKT activation. Key words: Clear-cell renal-cell carcinoma; PTEN; PI3K/ AKT pathway
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Objective To discuss the activity of the phosphatase and tensin homologue deleted on chromosome 10 (PTEN)/phosphatidylinositol 3-kinase (PI3K)/AKT pathway and the clinical significance of PTEN protein expression in clear-cell renal-cell carcinoma( CCRCC) tissues. Methods The protein of PTEN and AKT( phosphorylation at Ser473) of 36 paired CCRCC and adjacent non-neoplastic renal samples were analysed by Western blotting. Results The significantly increased AKT (phosphorylation at Ser473 ) with decreased PTEN protein were observed in CCRCC tissues compared with the adjacent non-neoplastic renal samples while the PTEN protein expression has no significant association with pathological parameters. Conclusion Our findings indicated that as PTEN dominantly inhibits AKT activation, the coexistence of high levels of the PTEN protein with enhanced AKT activation suggests the existence of novel mechanisms which attenuate PTEN function in CCRCC. These mechanisms may reduce PTEN function or increase AKT activation. Key words: Clear-cell renal-cell carcinoma; PTEN; PI3K/ AKT pathway
Key concepts: PTEN, Tensin, Protein kinase B, PI3K/AKT/mTOR pathway, Cancer research, Phosphorylation, Phosphatase, Biology