ABSTRACT
Objective@#The underlying mechanism of Ezrin in ovarian cancer (OVCA) is far from being understood. Therefore, this study aimed to assess the role of Ezrin in OVCA cells (SKOV3 and CaOV3) and investigate the associated molecular mechanisms.@*Methods@#We performed Western blotting, reverse transcription-quantitative polymerase chain reaction, MTT, cell colony, cell wound healing, transwell migration and invasion, RhoA and Rac active pull down assays, and confocal immunofluorescence experiments to evaluate the functions and molecular mechanisms of Ezrin overexpression or knockdown in the proliferation and metastasis of OVCA cells.@*Results@#The ectopic expression of Ezrin significantly increased cell proliferation, invasiveness, and epithelial-mesenchymal transition (EMT) in OVCA cells. By contrast, the knockdown of endogenous Ezrin prevented OVCA cell proliferation, invasiveness, and EMT. Lastly, we observed that Ezrin can positively regulate the active forms of RhoA rather than Rac-1 in OVCA cells, thereby promoting robust stress fiber formation.@*Conclusion@#Our results indicated that Ezrin regulates OVCA cell proliferation and invasiveness by modulating EMT and induces actin stress fiber formation by regulating Rho-GTPase activity, which provides novel insights into the treatment of the OVCA.
Subject(s)
Female , Humans , Cell Line, Tumor , Cell Movement , Cell Proliferation , Cytoskeletal Proteins/metabolism , Epithelial-Mesenchymal Transition , Gene Expression Regulation, Neoplastic , Neoplasm Invasiveness , Ovarian Neoplasms/pathology , Stress Fibers/metabolism , rhoA GTP-Binding Protein/metabolismABSTRACT
Objective To observe the expression changes of cytokine RhoA,stress fiber and Vinculin in the formation of hepatic fibrosis in rats, and investigate the role of RhoA in hepatic fibrosis. Methods Forty male SD rats were divided into two groups:model group and control group. The rats in the model group were given 60% CCl 4 by subcutaneous injection(1 ml/kg). The liver tissue was taken out for research at 1st、4th and 8th week respectively, RhoA and Vinculin mRNAs were detected by RT PCR, Vinculin and F actin proteins were detected by immunohistochemistry and immunofluorescence respectively, RhoA and Vinculin proteins were detected by Western blotting. Results Compared with control group, the expressions of mRNA of RhoA and Vinculin, the proteins of Vinculin, F actin and RhoA were all significantly increased( P
ABSTRACT
Theincreasedmicrovascularpermeabilityappearsmainlyinvenuleduringinflammation , shock ,andburns .Endothelialcellsplayanimportantroleinvenulepermeabilityenhancement.Therearetwo kindsofpathwayformacromoleculeextravasation .Oneisparacellularpathwayandanotheristranscellular pathway ,whicharerelatedtotheformationofendothelialgaportranscellularopeningsseperately .Thealter ationofintercellularrelatedprotein ,suchasoccludin ,claudin ,zonaoccludens (ZO) ,junctionaladhesion molecule (JAM) ,VE -cadherin ,catenin ,integrin ,etc ,andthealterationofendothelialcytoskeleton ,such asrearrangementofactinfilament,formationofstressfiberandfocaladhesion ,etc ,involveinthepathogenesis ofincreasedmicrovascularpermeability . [