scholarly journals miR-126 affects the invasion and migration of glioma cells through GATA4

2016 ◽  
Vol 45 (6) ◽  
pp. 1247-1253 ◽  
Author(s):  
Yifan Xu ◽  
Wu Xu ◽  
Tianyu Lu ◽  
Yuxiang Dai ◽  
Weibang Liang
Keyword(s):  
Glioma Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals GGNBP2 Suppresses the Proliferation, Invasion, and Migration of Human Glioma Cells

2017 ◽  
Vol 25 (5) ◽  
pp. 831-842 ◽  
Author(s):  
Ao Zhan ◽  
Bo Lei ◽  
Honggang Wu ◽  
YueTao Wen ◽  
Liandong Zheng ◽  
...  
Keyword(s):  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals The Effect of Ginger on the Invasion and Migration of Glioma Cells

2020 ◽  
pp. 38-43
Author(s):  
Manar Zraikat ◽  
Munir Gharaibeh ◽  
Tasneem Alshelleh
Keyword(s):  
Cell Line ◽  
Tumour Progression ◽  
Glioma Cells ◽  
Three Dimension ◽  
Scratch Assay ◽  
Invasion And Migration ◽  
Invasion Model ◽  
Dimension 2 ◽  
And Migration ◽  
U87 Cells

Background: This work studies the effect of different concentrations of soaked ginger on the ability of the U87 glioma cells to invade collagen in a three dimension (3 D) invasion model and compare it with its effect on the ability of the same cell line to migrate in two-dimension (2 D) scratch assay. Methods: The hanging drop spheroids in 3D invasion assay were used to investigate the in invasion of the U87 cells. The 2D scratch assay was used to investigate the migration of the same cell line. Results: Gradual effect of the soaked ginger was noticed on the inhibition of the invasion of U87 in collagen and on the inhibition of the migration of the same cell line in scratch assay. Conclusion: The results in this article are promising and encourage further studies to investigate the effect of ginger active ingredients on tumour progression.

scholarly journals TRIM31 promotes proliferation, invasion and migration of glioma cells through Akt signaling pathway

Neoplasma ◽  
2019 ◽  
Vol 66 (05) ◽  
pp. 727-735
Author(s):  
G. Shi ◽  
C. Lv ◽  
Z. Yang ◽  
T. Qin ◽  
L. Sun ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Glioma Cells ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Invasion And Migration ◽  
And Migration

scholarly journals miR-132 can inhibit glioma cells invasion and migration by target MMP16 in vitro

2015 ◽  
pp. 3211 ◽  
Author(s):  
You xin Zhou ◽  
Hangzhou Wang ◽  
Yan-yan Li ◽  
Zhi-wu Wu ◽  
Tian-quan Yang ◽  
...  
Keyword(s):  
Glioma Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Fraxetin Inhibits the Proliferation and Metastasis of Glioma Cells by Inactivating JAK2/STAT3 Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Liangchen Qu ◽  
Pan Lin ◽  
Minjie Lin ◽  
Shumin Ye ◽  
Percy David Papa Akuetteh ◽  
...  
Keyword(s):  
Chemical Reactivity ◽  
Glioma Cells ◽  
Migration And Invasion ◽  
Drug Candidate ◽  
Recurrence Rates ◽  
Invasion And Migration ◽  
Stat3 Signaling ◽  
Time Migration ◽  
And Migration

Glioma is the most common brain tumor and is characterized by high mortality rates, high recurrence rates, and short survival time. Migration and invasion are the basic features of gliomas. Thus, inhibition of migration and invasion may be beneficial for the treatment of patients with glioma. Due to its antitumor activity and chemical reactivity, fraxetin has attracted extensive interest and has been proven to be an effective antitumor agent in various cancer types. However, currently, the potential effects of fraxetin on glioma have not been investigated. Here, we demonstrate that fraxetin can inhibit the proliferation, invasion, and migration of glioma and induce apoptosis of glioma cells in vitro and in vivo. Therefore, these findings establish fraxetin as a drug candidate for glioma treatment. Furthermore, fraxetin was able to effectively inhibit the JAK2/STAT3 signaling in glioma. In summary, our results show that fraxetin inhibits proliferation, invasion, and migration of glioma by inhibiting JAK2/STAT3 signaling and inducing apoptosis of glioma cells. The present study provides a solid basis for the development of new glioma therapies.

scholarly journals CTR9-Mediated JAK2/STAT3 Pathway Promotes The Proliferation, Migration and Invasion of Human Glioma Cells

2021 ◽  
Author(s):  
Yang Xu ◽  
Jiaguo Chen ◽  
Gao He ◽  
Yuhai Zhang
Keyword(s):  
Protein Modification ◽  
Cell Function ◽  
Glioma Cells ◽  
Migration And Invasion ◽  
Stat3 Pathway ◽  
Invasion And Migration ◽  
The Public ◽  
Significant Difference ◽  
And Migration ◽  
U87 Cells

Abstract Background CTR9 (Cln three requiring 9) has been reported to be implicated in protein modification and oncogenesis of several human cancers. However, the protein expression and mechanism of CTR9 in glioma progression remain unclear. Methods We analyzed mRNA expression of CTR9 and CTR9-related survival curves in the public database. Then we detected CTR9 expression in glioma tissues and constructed U251 and U87 cells with stable silencing or overexpression of CTR9. Cell function tests and Western blot were conducted to explore the effects of CTR9 on glioma proliferation, invasion and migration, as well as the specific mechanism. All the date was presented as means ± SEM. Two-sample t-test and one-way analysis of variance (ANOVA) were used to identify whether there was a significant difference between each group of data. Results We found that CTR9 was overexpressed in glioma and inversely associated with glioma patient survival. The results manifested that knockdown of CTR9 suppressed the proliferation, migration and invasion of glioma cells, while overexpression facilitated them. The underlying molecular mechanism may involve the regulation of JAK2/STAT3 pathway by CTR9. Conclusion Our present study indicates that CTR9 is highly expressed in glioma and related to glioma grading and prognosis. CTR9 regulates malignant behaviors of glioma cells by activating JAK2/STAT3 pathway. Therefore, CTR9 is a promising biomarker for the diagnosis,targeted therapy and prognosis evaluation of glioma.

scholarly journals Long noncoding RNA OIP5-AS1 targets Wnt-7b to affect glioma progression via modulation of miR-410

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Wei-Li Sun ◽  
Tian Kang ◽  
Yuan-Yu Wang ◽  
Jian-Ping Sun ◽  
Chen Li ◽  
...  
Keyword(s):  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Biological Effects ◽  
Glioma Cells ◽  
Phase Cell ◽  
Luciferase Reporter ◽  
Invasion And Migration ◽  
Reporter Assays ◽  
And Migration ◽  
U87 Cells

Abstract The present study was undertaken to investigate the underlying mechanisms of long noncoding RNA OIP5-AS1 via regulating miR-410 to modulate Wnt-7b in the progression of glioma. To address this problem, we measured the expression of OIP5-AS1 and miR-410 in glioma tissues by qRT-PCR. Glioma U87 cells were transfected with OIP5-AS1 siRNA or miR-410 inhibitors. The targeting relationships among miR-410, OIP5-AS1 and Wnt-7b were verified by luciferase reporter assays. Western blotting was employed to determine the expression of Wnt-7b/β-catenin pathway-related proteins, while MTT, flow cytometry, Transwell assays and wound-healing assays were used to measure the biological characteristics of glioma cells. The results showed that OIP5-AS1 expression was higher and miR-410 was lower in glioma tissues. Luciferase reporter assays confirmed a targeting relationship between OIP5-AS1 and miR-410, as well as between miR-410 and Wnt-7b. Silencing OIP5-AS1 reduced cell proliferation, invasion and migration of glioma U87 cells and led to depressed expression levels of miR-410, Wnt-7b, p-β-catenin, GSK-3β-pS9, c-Myc and cyclin D1. Furthermore, down-regulation of OIP5-AS1 induced G0/G1 phase cell cycle arrest and apoptosis of glioma cells. Inhibitors of miR-410 abolished the biological effects of OIP5-AS1 siRNA in glioma cells. In vivo, OIP5-AS1 knockdown also inhibited tumor growth. Taken together, this research suggested that silencing OIP5-AS1 may specifically block the Wnt-7b/β-catenin pathway via targeted up-regulating miR-410, thereby inhibiting growth, invasion and migration while promoting apoptosis in glioma cells.

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