Knockdown of CLN5 inhibits the tumorigenic properties of glioblastoma cells via the Akt/mTOR signaling pathway
- Jiexia Xing
- Ying Li
- Huilan Zhao
Affiliations: Department of Neurology, Shandong University of Qilu Hospital, Jinan, Shandong 250012, P.R. China, Department of Critical Medicine, The Third People's Hospital of Heze, Heze, Shandong 274000, P.R. China, Department of Geriatrics, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250011, P.R. China
- Published online on: March 17, 2021 https://doi.org/10.3892/ol.2021.12648
Copyright: © Xing
et al. This is an open access article distributed under the
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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.