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Chinese Journal of Immunology ; (12): 675-680, 2018.
Article in Chinese | WPRIM | ID: wpr-702796

ABSTRACT

Objective:To investigate the effect of PKM2 on proliferation and apoptosis of nasopharyngeal carcinoma cells.Methods:Nasopharyngeal carcinoma cell CNE-1 was transfected with PKM2 small interfering RNA (PKM2 siRNA1 and PKM2 siRNA2) and negative controls (siRNA control),the levels of PKM2 in the cells were detected by fluorescent quantitative PCR and Western blot,screening interference PKM2 siRNA2 continued to study.Cell proliferation was detected by MTT,cell cloning test showed the ability of cell cloning,apoptosis was detected by flow cytometry,ROS level was detected by DCFH-DA,the levels of p38MAPK,p-p38MAPK,C-myc,β-catenin,Cleaved Caspase-3 protein were detected by Western blot.Results:After transfection of PKM2 siRNA1 and PKM2 siRNA2,the levels of PKM2 mRNA and protein were significantly decreased compared with those without transfection,and after transfection of PKM2 siRNA2,the level of PKM2 in cells decreased more,the levels of PKM2 in transfected siRNA control cells were not significantly different from those without transfection.The rate of apoptosis after down-regulation of PKM2 expression increased from (9.36 ± 1.04)% to (48.42 ± 5.28)%,and the rate of cell clone formation decreased from (75.48 ± 8.25)% to (46.15 ± 3.47)%,OD values from (0.86±0.11) down to (0.52±0.04),elevated levels of ROS in cells,the levels of p-p38MAPK,Cleaved Caspase-3 proteins in cells were also significantly increased, the levels of C-myc and β-catenin in cells were obviously decreased.Conclusion:Downregulation of PKM2 expression inhibits nasopharyngeal carcinoma cell growth,promoting apoptosis of naso-pharyngeal carcinoma cells,the mechanism of action may be related to p38MAPK and Wnt/β-catenin signaling pathway.

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