The Role of P TEN Protein Phosphatase in Nasopharyngeal Carcinoma: The Ability of TGF-β1 Inducing Migration and Invasion was Inhibited by PTEN Protein Phosphatase through Down-regulating p-P38

crossref(2020)

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摘要
Abstract BackgroundThe phosphatase and tensin homolog gene(PTEN) is a crucial cancersuppressor gene in nasopharyngeal carcinoma(NPC),which encodes the protein i-ncluding lipid phosphatase and protein phosphatase.p-P38 plays a vital role in the development process of cancers.However,whether and how PTEN protein p-hosphatase inhibit p-P38 expression and regulate migration and invasion in nas-opharyngeal carcinoma is still fully elucidated.MethodsThe abilities of migration and invasion were analyzed using Scratch,Transwell,Boyden experiments in NPC cells.Westere Blot was utilized to explo-re the expression of E-caherin,N-caherin and VIMENTIN in Epithelial-mesench-ymal transition(EMT),P38,p-P38(Thr180/Tyr182),AKT,p-AKT(Ser473),PTEN and its mutants.qPCR was done to detect the mRNA expression of PTEN and PTEN mutants.Immunofluorescence localization assay and Co-immunoprecipitatio-n assay was used to explore the mutual combination of PTEN and P38.ResultsWe verified that transforming growth factor-β1(TGF-β1) could induce migration,invasion,and EMT in NPC again,and appropriate concentration was 5ng/ml.Interesting,we demonstrated that 5ng/ml TGF-β1 enhanced the level of p-AKT(Ser473)and p-P38(Thr180/Tyr182).Further more,after overexpression of PTEN WT and various mutants including PTEN-C124S(lacking of both lipid p-hosphatase and protein phosphatase),PTEN-G129E(only lacking of lipid phosph-atase but remaining protein phosphatase),PTEN-Y138L(lacking of protein phosp-hatase but remaining lipid phosphatase),and PTEN 1-353(Lack of c-tail structur-e),we observed that PTEN protein phosphatase reduced the ability of migration,invasion by inhibiting TGF-β1-induced p-P38,but the PTEN c-tail did not invo-lvein this process.At last,we confirmed PTEN could bind to P38 each other.ConclusionsThe asssys in the study indicated that PTEN protein phosphatasemight be anticancer,where it was able to inhibit the ability of TGF-β1 inducingmigration and invasion by reducing p-P38 in NPC cells.
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