Silibinin Inhibits Glioma Cell Proliferation via Ca2+/ROS/MAPK-Dependent Mechanism In Vitro and Glioma Tumor Growth In Vivo

2009 ◽  
Vol 34 (8) ◽  
pp. 1479-1490 ◽  
Author(s):  
Kwang Won Kim ◽  
Chang Hwa Choi ◽  
Thae Hyun Kim ◽  
Chae Hwa Kwon ◽  
Jae Suk Woo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Glioma Cell ◽  
Glioma Cell Proliferation ◽  
Glioma Tumor ◽  
Dependent Mechanism

scholarly journals circ_0030018 promotes glioma proliferation and metastasis

2021 ◽  
Vol 12 (1) ◽  
pp. 260-272
Author(s):  
Yun Shao ◽  
Zhengxiang Yang ◽  
Weifeng Miao ◽  
Xiangrong Yu ◽  
Yiping Wu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Glioma Cell ◽  
Animal Experiments ◽  
Circular Rna ◽  
Luciferase Reporter ◽  
Cell Progression ◽  
Glioma Cell Proliferation ◽  
Glioma Tumor

Abstract Background Circular RNA (circRNA) plays an essential role in tumor progression, including glioma. circ_0030018 is a newly discovered circRNA that is highly expressed in glioma. However, its role and mechanism in glioma need to be further elucidated. Methods The expression of circ_0030018, microRNA (miR)-194-5p, and tripartite motif containing 44 (TRIM44) was examined using quantitative real-time PCR. Cell proliferation, migration, invasion, and apoptosis were determined using MTT assay, colony formation assay, transwell assay, and flow cytometry. Moreover, dual-luciferase reporter assay and RNA pull-down assay were used to verify the interactions among circ_0030018, miR-194-5p, and TRIM44. The protein expression of TRIM44 was assessed by western blot analysis. Animal experiments were conducted to explore the role of circ_0030018 in glioma tumor growth in vivo. Results circ_0030018 was overexpressed in glioma tissues and cells, and its silencing could inhibit glioma cell proliferation, migration, invasion, and accelerate apoptosis. miR-194-5p could be sponged by circ_0030018, and its overexpression could hinder the progression of glioma cells. Further experiments revealed that miR-194-5p inhibitor reversed the negative regulation of circ_0030018 knockdown on glioma cell progression. In addition, TRIM44 was a target of miR-194-5p, and its downregulation could repress glioma cell progression. Overexpressed TRIM44 reversed the inhibition effect of miR-194-5p on glioma cell progression. Animal experiments suggested that circ_0030018 knockdown could reduce glioma tumor growth through regulating miR-194-5p and TRIM44. Conclusion Our 8data showed that circ_0030018 enhanced glioma progression by sponging miR-194-5p to regulate TRIM44, indicating that circ_0030018 might be a potential treatment target for glioma.

scholarly journals ACT001, a novel PAI-1 inhibitor, exerts synergistic effects in combination with cisplatin by inhibiting PI3K/AKT pathway in glioma

2019 ◽  
Vol 10 (10) ◽  
Author(s):  
Xiaonan Xi ◽  
Ning Liu ◽  
Qianqian Wang ◽  
Yahui Chu ◽  
Zheng Yin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Synergistic Effect ◽  
Glioma Cell ◽  
Synergistic Effects ◽  
Akt Pathway ◽  
Phase I Clinical Trials ◽  
Glioma Cell Proliferation ◽  
Pai 1

Abstract PAI-1 plays significant roles in cancer occurrence, relapse and multidrug resistance and is highly expressed in tumours. ACT001, which is currently in phase I clinical trials for the treatment of glioblastoma (GBM). However, the detailed molecular mechanism of ACT001 is still unclear. In this study, we investigated the effects of ACT001 on glioma cell proliferation and clarified its mechanism. We discovered that PAI-1 was the direct target of ACT001 by a cellular thermal shift assay. Then, the interaction between ACT001 and PAI-1 was verified by Biacore assays, thermal stability assays and ACT001 probe assays. Furthermore, from the proteomic analysis, we found that ACT001 directly binds PAI-1 to inhibit the PI3K/AKT pathway, which induces the inhibition of glioma cell proliferation, invasion and migration. Moreover, the combination of ACT001 and cisplatin showed a synergistic effect on the inhibition of glioma in vitro and in vivo. In conclusion, our findings demonstrate that PAI-1 is a new target of ACT001, the inhibition of PAI-1 induces glioma inhibition, and ACT001 has a synergistic effect with cisplatin through the inhibition of the PAI-1/PI3K/AKT pathway.

402 The endogenous EPO/EPOR system contributes to glioma cell proliferation both in vitro and in vivo

2010 ◽  
Vol 8 (5) ◽  
pp. 103
Author(s):  
E. Pérès ◽  
S. Valable ◽  
J.S. Guillamo ◽  
J.F. Bernaudin ◽  
S. Roussel ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Glioma Cell Proliferation

ZFX regulates glioma cell proliferation and survival in vitro and in vivo

2013 ◽  
Vol 112 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Zhichuan Zhu ◽  
Kui Li ◽  
Dafeng Xu ◽  
Yongjie Liu ◽  
Hailiang Tang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Glioma Cell Proliferation

scholarly journals TCTP promotes glioma cell proliferation in vitro and in vivo via enhanced  -catenin/TCF-4 transcription

2013 ◽  
Vol 16 (2) ◽  
pp. 217-227 ◽  
Author(s):  
X. Gu ◽  
L. Yao ◽  
G. Ma ◽  
L. Cui ◽  
Y. Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Glioma Cell Proliferation ◽  
Proliferation In Vitro

scholarly journals PPARα Regulates the Proliferation of Human Glioma Cells through miR-214 and E2F2

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yong Gao ◽  
Dongfeng Han ◽  
Laisheng Sun ◽  
Qihua Huang ◽  
Guangchao Gai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Nuclear Hormone Receptor ◽  
Low Grade ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Anaplastic Gliomas ◽  
Glioma Cell Proliferation

Peroxisome proliferator-activated receptor α (PPARα) is a member of the nuclear hormone receptor superfamily and functions as a transcription factor. Previous work showed that PPARα plays multiple roles in lipid metabolism in tissues such as cardiac and skeletal muscle, liver, and adipose tissue. Recent studies have discovered additional roles for PPARα in cell proliferation and metabolism, as well as tumor progression. PPARα is aberrantly expressed in various cancers, and activated PPARα inhibits the proliferation of some tumor cells. However, there have been no studies of PPARα in human gliomas. Here, we show that PPARα is expressed at lower levels in anaplastic gliomas and glioblastoma multiforme (GBM) tissue compared with low-grade gliomas tissue, and low expression is associated with poor patient prognosis. PPARα activates transcription of dynamin-3 opposite strand (DNMO3os), which encodes a cluster of miR-214, miR-199a-3p, and miR-199a-5p microRNAs. Of these, miR-214 is transcribed at particularly high levels. PPARα-induced miR-214 expression causes downregulation of its target E2F2. Finally, miR-214 overexpression inhibits glioma cell growth in vitro and in vivo by inducing cell cycle arrest in G0/G1. Collectively, these data uncover a novel role for a PPARα-miR-214-E2F2 pathway in controlling glioma cell proliferation.

scholarly journals GSK1838705A, an IGF-1R inhibitor, inhibits glioma cell proliferation and suppresses tumor growth in vivo

2015 ◽  
Vol 12 (4) ◽  
pp. 5641-5646 ◽  
Author(s):  
XIANG ZHOU ◽  
FAZHENG SHEN ◽  
PENGJU MA ◽  
HONGYAN HUI ◽  
SUJUAN PEI ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Glioma Cell ◽  
Glioma Cell Proliferation
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