Abstract：Abstract: Using anisomycin to activate JNK in glioma U251 cells, the antitumor effect of activated JNK on glioma was investigated, and the key transcription factor regulated by JNK was found. This paper uses an online analysis website to predict a tumor model regulated by JNK; through the use of anisemycin (JNK agonist), the effective regulation of intracellular P-JNK levels was achieved, and its optimal conditions are explored by Western blot experiments; through experiments such as CCK-8 detection, cell counting, cell scratching, and flow cytometry the effects of activated JNK on the cell proliferation, migration, and cell cycle of U251 cells were explored; RNA-seq analysis was used to find the key transcription factor regulated by JNK. The results show that, there is a strong correlation between JNK and the occurrence and development of gliomas through bioinformatics data analysis；after 1.0 h of 1.0μg/mL anisemycin, it can effectively activate the endogenous JNK activity of glioma U251 cells, inhibit cell proliferation and migration, and cause cell cycle arrest; RNA-seq analysis revealed that JNK may inhibit the growth of gliomas by regulating the activity of P53. This paper found that activating JNK can produce a tumor suppressive effect on gliomas, and it will provide a basis of JNK as a therapeutic target for gliomas; P53, the transcription factors found by RNA-seq analysis, that also provide a direction for further exploring the mechanism between JNK and the development of gliomas.
Key words: JNK; glioma cell U251; antitumor effect; RNA-seq; anisomycin
引用本文:
姜瑞芬，谭拥军，黄明敏. 激活JNK后对神经胶质瘤抑瘤效果的探究[J]. 激光生物学报, 2020, 29(5): 453-460.
JIANG Ruifen, TAN Yongjun, HUANG Mingmin. A Study on the Antitumor Effects of Glioma by Activated JNK. journal1, 2020, 29(5): 453-460.
