Knockdown of CLN5 inhibits the tumorigenic properties of glioblastoma cells via the Akt/mTOR signaling pathway |
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| Authors: | Jiexia Xing Ying Li Huilan Zhao |
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| Institution: | 1.Department of Neurology, Shandong University of Qilu Hospital, Jinan, Shandong 250012, P.R. China;2.Department of Critical Medicine, The Third People''s Hospital of Heze, Heze, Shandong 274000, P.R. China;3.Department of Geriatrics, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250011, P.R. China |
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| Abstract: | Gliomas are highly malignant tumors with a rapid progression and poor prognosis. The present study investigated the cellular effects of CLN5-knockdown in the glioblastoma (GBM) U251 and U87MG cell lines. The Cell Counting Kit-8 and colony formation assays indicated that CLN5-knockdown inhibited the proliferation of GBM cells. Additionally, the results of the Transwell and scratch assays revealed that CLN5-knockdown significantly inhibited migration and invasion, and the flow cytometry analysis confirmed that apoptosis was promoted. Knockdown of CLN5 downregulated the expression levels of MMP-2, Bcl-2, cyclin D1, CDK4 and CDK6, and upregulated the expression levels of Bax and activated caspase-9. Additionally, it blocked GBM cells in the G1-phase and induced early apoptosis. Knockdown of CLN5 inhibited the activation of the Akt and mTOR signaling pathways in GBM by decreasing the levels of phosphorylated (p)-Akt and p-mTOR. The present data suggested that downregulation of CLN5 may be a potential treatment option for GBM. Knockdown of CLN5 inhibited the development of GBM via the inhibition of the Akt and mTOR signaling pathways. |
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| Keywords: | CLN5 glioblastoma U251 U87MG Akt/mTOR pathway apoptosis |
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