Ski regulates proliferation and migration of reactive astrocytes induced by lipopolysaccharide (LPS) through PI3K/Akt pathway

2022 ◽  
pp. 577807
Author(s):  
Hai-Yang Liao ◽  
Zhi-qiang Wang ◽  
Chao-Ming Da ◽  
Kai-Sheng Zhao ◽  
Hai-hong Zhang
Keyword(s):  
Reactive Astrocytes ◽  
Akt Pathway ◽  
And Migration ◽  
Proliferation And Migration

LncRNA ZFAS1 promotes proliferation and migration and inhibits apoptosis in nasopharyngeal carcinoma via the PI3K/AKT pathway in vitro

2019 ◽  
Vol 26 (2) ◽  
pp. 171-182 ◽  
Author(s):  
Xiaoqiong Wang ◽  
Qiaozhi Jin ◽  
Xue Wang ◽  
Wubing Chen ◽  
Zhiyi Cai
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Akt Pathway ◽  
And Migration ◽  
Proliferation And Migration

LINC00893 inhibits papillary thyroid cancer by suppressing AKT pathway via stabilizing PTEN

2020 ◽  
pp. 1-10
Author(s):  
Shujing Li ◽  
Yanyan Zhang ◽  
Jian Dong ◽  
Ruihuan Li ◽  
Bo Yu ◽  
...  
Keyword(s):  
Akt Pathway ◽  
Phosphatase And Tensin Homolog ◽  
Fused In Sarcoma ◽  
Tensin Homolog ◽  
Phosphorylated Akt ◽  
Pten Mrna ◽  
Non Coding Rnas ◽  
And Migration ◽  
Fus Protein ◽  
Proliferation And Migration

Long non-coding RNAs (lncRNAs) are important to the occurrence and advancement of human cancers. We found through GEPIA that LINC00893 was lowly expressed in thyroid carcinoma (THCA) tissues, whereas the specific functions of LINC00893 has never been reported in PTC. In the current study, we confirmed that LINC00893 was expressed at a low level in PTC cells. Through gain-of-function assays, we determined that LINC00893 overexpression abrogated proliferation and migration abilities of PTC cells. Through signal transduction reporter array we found that LINC00893 potentially modulated the signals of phosphatase and tensin homolog (PTEN)/AKT pathway. In addition, overexpression of LINC00893 increased the expression of PTEN but reduced the levels of phosphorylated AKT in PTC. Additionally, mechanism assays unveiled that LINC00893 stabilized PTEN mRNA via recruiting Fused in sarcoma (FUS) protein. Finally, rescue assays demonstrated that LINC00893 hampered the proliferation and migration of PTC cells via PTEN/AKT pathway. Together, our study first clarified that LINC00893 functions as a tumor suppressor in PTC by blocking AKT pathway through PTEN upregulation.

Increased LGALS3BP promotes proliferation and migration of oral squamous cell carcinoma via PI3K/AKT pathway

2019 ◽  
Vol 63 ◽  
pp. 109359 ◽  
Author(s):  
Xiaoxin Zhang ◽  
Haoyue Ding ◽  
Zhanyi Lu ◽  
Liang Ding ◽  
Yuxian Song ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Akt Pathway ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Carnosine suppresses oxygen-glucose deprivation/recovery-induced proliferation and migration of reactive astrocytes of rats in vitro

2017 ◽  
Vol 39 (1) ◽  
pp. 24-34 ◽  
Author(s):  
Li Ou-yang ◽  
Yuan Liu ◽  
Bing-yu Wang ◽  
Pei Cao ◽  
Jing-jing Zhang ◽  
...  
Keyword(s):  
Glucose Deprivation ◽  
Reactive Astrocytes ◽  
Oxygen Glucose Deprivation ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals GATA1 Gene Silencing Inhibits Invasion, Proliferation and Migration of Cholangiocarcinoma Stem Cells via Disrupting the PI3K/AKT Pathway [Retraction]

2021 ◽  
Vol Volume 14 ◽  
pp. 1005-1006
Author(s):  
Guang Shi ◽  
Hong Zhang ◽  
Qiong Yu ◽  
Chunmei Hu ◽  
Youbo Ji
Keyword(s):  
Stem Cells ◽  
Gene Silencing ◽  
Akt Pathway ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals EGCG inhibited bladder cancer T24 and 5637 cell proliferation and migration via PI3K/AKT pathway

Oncotarget ◽  
2018 ◽  
Vol 9 (15) ◽  
pp. 12261-12272 ◽  
Author(s):  
Ke-Wang Luo ◽  
Wing-Yin Lung ◽  
Chun-Xie ◽  
Xin-Le Luo ◽  
Wei-Ren Huang
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Akt Pathway ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals DHI increases the proliferation and migration of Schwann cells through PI3K/AKT pathway and the expression of CXCL12 and GDNF to promote facial nerve function repair

2021 ◽  
Author(s):  
Dekun Gao ◽  
Lianhua Sun ◽  
Xiayu Sun ◽  
Jun Yang ◽  
Jingchun He
Keyword(s):  
Facial Nerve ◽  
Western Blot ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Akt Pathway ◽  
Nerve Function ◽  
Facial Nerve Function ◽  
Facial Nerve Injury ◽  
And Migration ◽  
Proliferation And Migration

Abstract BackgroundDanhong injection (DHI) is a commonly used drug in the treatment of cardiovascular and cerebrovascular diseases, and its neuroprotective research has been fully confirmed. Schwann cells, as myelin forming cells of peripheral nerve, play an important role in the process of injury and repair. The purpose of this study was to explore the effect of DHI on Schwann cells and its role in facial nerve injury.MethodsRSC 96 Schwann cells were treated with different concentrations (0 –2%) of DHI for different time intervals (12 and 36 h). Effect of DHI on cell viability and migration were determined by CCK8 and Transwell assays. The levels of PI3K-Akt signaling related proteins were measured by western blotting analysis, and the effects of DHI on GDNF and CXCL12 using Western Blot, RT-qPCR, and ELISA assays at the cellular and animal levels, respectively. Then LY294002, an inhibitor of PI3K, was used to study the effect of DHI on cell migration and secretion of CXCL12 and GDNF in RSC96 cells by Transwell, Western Blot, RT-qPCR, and ELISA assays. Finally, facial nerve scoring and S-100 immunofluorescence staining were used to study the therapeutic effects of DHI on facial nerve injury.ResultsOur study found that DHI can promote the proliferation and migration of RSC96 cells, and this effect is related to the activation of PI3K/AKT pathway. LY294002 inhibits the proliferation and migration of RSC96 cells. Besides, DHI can also promote the expression of CXCL12 and GDNF at gene and protein levels, and CXCL12 is, while GDNF is not, PI3K/AKT pathway-dependent. Animal experiments confirmed that DHI could promote CXCL12 and GDNF expression, and promote facial nerve function recovery and myelin regeneration. Conclusion Our in vitro and in vivo experiments demonstrated that DHI could promote proliferation and migration of Schwann cells through the PI3K/AKT pathway, and increase the expression of CXCL12 and GDNF to promote facial nerve function repair.

Sign in / Sign up

Export Citation Format

Share Document