ERK5 inhibitor XMD17-109 inhibits glioma progression by down-regulating ITPRIP expression / 重庆医学
Chongqing Medicine
; (36): 3546-3553, 2023.
Article
de Zh
| WPRIM
| ID: wpr-1017406
Bibliothèque responsable:
WPRO
ABSTRACT
Objective To investigate the effect of XMD17-109 on the viability of glioma cells and its molecular mechanism based on extracellular signal-regulated kinase 5(ERK5)/inositol 1,4,5-trisphosphate receptor-interacting protein(ITPRIP)signaling pathway.Methods U251 glioma cells were routinely cul-tured,and ERK5 activity was inhibited by XMD17-109.ERK5 knockdown and ERK5 overexpression models were constructed by transfection of RNA fragments and plasmids,respectively.Cells were divided divided into the XMD17-109 group,the Control group,the siERK5 group,the siNC group,siERK5-OE group,the Vector group,the ERK5-OE+XMD17-109 group and the Vector+XMD17-109 group.The cell viability was detected by CCK-8,scratch and flow cytometry experiments and so on.The mRNA and protein expression levels of ERK5 and ITPRIP were detected by reverse transcription-quantitative real time PCR(RT-qPCR)and West-ern blot.Results Compared with the Control group,the cell viability of the XMD17-109 group decreased,and the expression level of ITPRIP decreased(P<0.05).Compared with the siNC group,the cell viability of the siERK5 group was decreased,and the expression level of ITPRIP was decreased(P<0.05).Compared with the Vector group,the cell viability of the ERK5-OE group was enhanced,and the expression level of ITPRIP was increased(P<0.05).Compared the with Vector+XMD17-109 group,the cell viability of the ERK5-OE+XMD17-109 group was enhanced,and the expression level of ITPRIP was increased(P<0.05).Conclusion XMD17-109 can inhibit the viability of glioma cells by inhibiting ERK5/ITPRIP signaling pathway,which is expected to be a potential drug for glioma treatment.
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Indice:
WPRIM
langue:
Zh
Texte intégral:
Chongqing Medicine
Année:
2023
Type:
Article