AIM:To evaluate the effect of miRNA-451 on rhesus macaque choroid-retinal endothelial(RF/6A)cell function and proteome profile.METHODS:The RF/6A cells were transfected with miRNA-451 mimic and inhibitor.The role of mi...AIM:To evaluate the effect of miRNA-451 on rhesus macaque choroid-retinal endothelial(RF/6A)cell function and proteome profile.METHODS:The RF/6A cells were transfected with miRNA-451 mimic and inhibitor.The role of miRNA-451 on proliferation ability was evaluated by CCK-8 assay.Furthermore,iTRAQ quantitative proteomic analysis was applied to comprehensively illuminate the change of cellular proteins and biological function between different groups.RESULTS:In miRNA-451 overexpression group,cell proliferation of RF/6A decreased both at 24 h and 48 h;while in miRNA-451 inhibition group,on the contrary,RF/6A cell proliferation was increased at 48 h.Based on iTRAQ quantitative proteomic analysis,23 differentially expressed proteins(DEPs)were detected in the comparison of miRNA-451 mimic and mimic control-transfected RF/6A cells,and 30 DEPs were identified in the comparison of RF/6A cells transfected with miRNA-451 inhibitor and inhibitor control.DEPs such as GORASP2,KRT1,SLC7 A2,RIC8 A,DDX42,CAP1,PCBP2 might be closely related to the inhibitory effect of miRNA-451 on RF/6A cell proliferation,while PCYT1 A,MGAT1,TUBB,MCU,SIL1,BID,MSH6 might account for the positive effect of miRNA-451 inhibitor on RF/6A cell growth.PTPN1,as the only protein exhibiting an opposite trend between miRNA-451 mimic and inhibitortransfected cells,was most likely accountable for the inhibition of miRNA-451 mimic on RF/6A cell growth,and the promotion of miRNA-451 inhibitor on RF/6A cell proliferation.CONCLUSION:miRNA-451 overexpression can suppress the growth of RF/6A cells while knockdown of miRNA-451 can promote RF/6A cell viability.Among all DEPs,increased PTPN1 is most likely to account for the negative regulation of miRNA-451 on RF/6A proliferation.miRNA-451 can be a protective factor for neovascular disease of fundus via regulating choroid retinal endothelial cell function.展开更多
Phosphatases are enzymes that remove phosphate groups from proteins and other molecules,playing a critical role in regulating various cellular processes.They act as key switches in cell signaling pathways,controlling ...Phosphatases are enzymes that remove phosphate groups from proteins and other molecules,playing a critical role in regulating various cellular processes.They act as key switches in cell signaling pathways,controlling cell cycle progression,gene expression,and cell growth1,2.In cancer,phosphatases can act as tumor suppressors or promoters.For example,PTPN2 and PTPN1 negatively regulate inflammation and immune cell function.Their loss in tumors or immune cells can enhance tumor immunoevasion and create an immunosuppressive microenvironment3.The CDC25 phosphatase family(CDC25A,B,and C)regulates cell cycle transitions by activating CDKs through dephosphorylation.CDC25A is particularly important for CDK2–cyclin A and CDK2–cyclin E activation at the G1/S transition and plays a role in G2/M phase transitions.The abnormal expression or function of these phosphatases is associated with uncontrolled cell proliferation,apoptosis resistance,and altered tumor microenvironments,making them promising targets for cancer therapy4,5.展开更多
基金Supported by grants from National Natural Science Foundation of China(No.81900891)Global Ophthalmology Awards Program 2020(No.482667)。
文摘AIM:To evaluate the effect of miRNA-451 on rhesus macaque choroid-retinal endothelial(RF/6A)cell function and proteome profile.METHODS:The RF/6A cells were transfected with miRNA-451 mimic and inhibitor.The role of miRNA-451 on proliferation ability was evaluated by CCK-8 assay.Furthermore,iTRAQ quantitative proteomic analysis was applied to comprehensively illuminate the change of cellular proteins and biological function between different groups.RESULTS:In miRNA-451 overexpression group,cell proliferation of RF/6A decreased both at 24 h and 48 h;while in miRNA-451 inhibition group,on the contrary,RF/6A cell proliferation was increased at 48 h.Based on iTRAQ quantitative proteomic analysis,23 differentially expressed proteins(DEPs)were detected in the comparison of miRNA-451 mimic and mimic control-transfected RF/6A cells,and 30 DEPs were identified in the comparison of RF/6A cells transfected with miRNA-451 inhibitor and inhibitor control.DEPs such as GORASP2,KRT1,SLC7 A2,RIC8 A,DDX42,CAP1,PCBP2 might be closely related to the inhibitory effect of miRNA-451 on RF/6A cell proliferation,while PCYT1 A,MGAT1,TUBB,MCU,SIL1,BID,MSH6 might account for the positive effect of miRNA-451 inhibitor on RF/6A cell growth.PTPN1,as the only protein exhibiting an opposite trend between miRNA-451 mimic and inhibitortransfected cells,was most likely accountable for the inhibition of miRNA-451 mimic on RF/6A cell growth,and the promotion of miRNA-451 inhibitor on RF/6A cell proliferation.CONCLUSION:miRNA-451 overexpression can suppress the growth of RF/6A cells while knockdown of miRNA-451 can promote RF/6A cell viability.Among all DEPs,increased PTPN1 is most likely to account for the negative regulation of miRNA-451 on RF/6A proliferation.miRNA-451 can be a protective factor for neovascular disease of fundus via regulating choroid retinal endothelial cell function.
基金supported by the Key Research and Development Program,Ministry of Science and Technology of the People’s Republic of China(No.2023YFC2606500).
文摘Phosphatases are enzymes that remove phosphate groups from proteins and other molecules,playing a critical role in regulating various cellular processes.They act as key switches in cell signaling pathways,controlling cell cycle progression,gene expression,and cell growth1,2.In cancer,phosphatases can act as tumor suppressors or promoters.For example,PTPN2 and PTPN1 negatively regulate inflammation and immune cell function.Their loss in tumors or immune cells can enhance tumor immunoevasion and create an immunosuppressive microenvironment3.The CDC25 phosphatase family(CDC25A,B,and C)regulates cell cycle transitions by activating CDKs through dephosphorylation.CDC25A is particularly important for CDK2–cyclin A and CDK2–cyclin E activation at the G1/S transition and plays a role in G2/M phase transitions.The abnormal expression or function of these phosphatases is associated with uncontrolled cell proliferation,apoptosis resistance,and altered tumor microenvironments,making them promising targets for cancer therapy4,5.
