Knockdown of CLN5 inhibits the tumorigenic properties of glioblastoma cells via the Akt/mTOR signaling pathway.

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.