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CLN5基因敲低通过Akt/mTOR信号通路抑制胶质母细胞瘤细胞的致瘤特性。

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

作者信息

Xing Jiexia, Li Ying, Zhao Huilan

机构信息

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.

出版信息

Oncol Lett. 2021 May;21(5):387. doi: 10.3892/ol.2021.12648. Epub 2021 Mar 17.

DOI:10.3892/ol.2021.12648
PMID:33777210
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7988714/
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.

摘要

神经胶质瘤是具有快速进展和不良预后的高度恶性肿瘤。本研究调查了在胶质母细胞瘤（GBM）U251和U87MG细胞系中敲低CLN5的细胞效应。细胞计数试剂盒-8和集落形成试验表明，敲低CLN5可抑制GBM细胞的增殖。此外，Transwell和划痕试验结果显示，敲低CLN5可显著抑制迁移和侵袭，流式细胞术分析证实促进了细胞凋亡。敲低CLN5可下调MMP-2、Bcl-2、细胞周期蛋白D1、CDK4和CDK6的表达水平，并上调Bax和活化的caspase-9的表达水平。此外，它使GBM细胞停滞在G1期并诱导早期凋亡。敲低CLN5通过降低磷酸化（p）-Akt和p-mTOR的水平抑制GBM中Akt和mTOR信号通路的激活。目前的数据表明，下调CLN5可能是GBM的一种潜在治疗选择。敲低CLN5通过抑制Akt和mTOR信号通路抑制GBM的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/6d252a1ad57c/ol-21-05-12648-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/b3bf33f841fa/ol-21-05-12648-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/e50fc266b70a/ol-21-05-12648-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/13125cb63a03/ol-21-05-12648-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/eea842c10b78/ol-21-05-12648-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/ec68d4e3943d/ol-21-05-12648-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/6d252a1ad57c/ol-21-05-12648-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/b3bf33f841fa/ol-21-05-12648-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/e50fc266b70a/ol-21-05-12648-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/13125cb63a03/ol-21-05-12648-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/eea842c10b78/ol-21-05-12648-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/ec68d4e3943d/ol-21-05-12648-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bf4/7988714/6d252a1ad57c/ol-21-05-12648-g05.jpg

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