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LKB1通过抑制NF-κB/蜗牛信号通路抑制胶质瘤细胞侵袭。

LKB1 suppresses glioma cell invasion via NF-κB/Snail signaling repression.

作者信息

Yuan Ye, Li Shi-Lin, Cao Yu-Lin, Li Jun-Jun, Wang Qiang-Ping

机构信息

Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, People's Republic of China,

Department of Neurology, Qitaihe Qimei Hospital, Qitaihe 154600, People's Republic of China.

出版信息

Onco Targets Ther. 2019 Apr 2;12:2451-2463. doi: 10.2147/OTT.S193736. eCollection 2019.

DOI:10.2147/OTT.S193736
PMID:31040689
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6452796/
Abstract

BACKGROUND

Liver kinase B1 (LKB1) is involved in various human diseases. Aberrant expression of LKB1 expression is involved in glioma progression and associated with prognosis, however, the specific mechanism involving NF-κB/Snail signaling pathways remain unknown.

MATERIALS AND METHODS

In the present study, quantitative real-time PCR analysis was used to investigate the expression of LKB1 tumor tissue samples and cell lines. In glioma cell lines, CCK-8 assay, transwell invasion and migration assays were used to investigate the effects of LKB1on proliferation and invasion.

RESULTS

We observed that LKB1 knockdown promoted glioma cell proliferation, migration and invasion. This effect was induced through NF-κB/Snail signaling activation. Also, LKB1 overexpression suppressed proliferation, migration, and invasion, which could be rescued by Snail overexpression.

CONCLUSION

Taken together, our results show that LKB1 knockdown promotes remarkably glioma cell proliferation, migration and invasion by regulating Snail protein expression through activating the NF-κB signaling. This may serve as a potential prognostic marker and therapeutic target for glioma.

摘要

背景

肝脏激酶B1（LKB1）参与多种人类疾病。LKB1表达异常与胶质瘤进展有关并与预后相关，然而，涉及核因子κB/蜗牛（NF-κB/Snail）信号通路的具体机制仍不清楚。

材料与方法

在本研究中，采用定量实时聚合酶链反应分析来研究LKB1在肿瘤组织样本和细胞系中的表达。在胶质瘤细胞系中，使用细胞计数试剂盒-8（CCK-8）检测、Transwell侵袭和迁移检测来研究LKB1对增殖和侵袭的影响。

结果

我们观察到LKB1基因敲低促进胶质瘤细胞增殖、迁移和侵袭。这种效应是通过NF-κB/Snail信号激活诱导的。此外，LKB1过表达抑制增殖、迁移和侵袭，而蜗牛蛋白（Snail）过表达可挽救这种抑制作用。

结论

综上所述，我们的结果表明，LKB1基因敲低通过激活NF-κB信号调节Snail蛋白表达，显著促进胶质瘤细胞增殖、迁移和侵袭。这可能作为胶质瘤潜在的预后标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2a0/6452796/715f0b294f44/ott-12-2451Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2a0/6452796/252a67bb658a/ott-12-2451Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2a0/6452796/94899a9b1b46/ott-12-2451Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2a0/6452796/fb582db4aa7a/ott-12-2451Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2a0/6452796/a4e8d744ddd2/ott-12-2451Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2a0/6452796/715f0b294f44/ott-12-2451Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2a0/6452796/252a67bb658a/ott-12-2451Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2a0/6452796/94899a9b1b46/ott-12-2451Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2a0/6452796/fb582db4aa7a/ott-12-2451Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2a0/6452796/a4e8d744ddd2/ott-12-2451Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2a0/6452796/715f0b294f44/ott-12-2451Fig5.jpg

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