scholarly journals Effects of Enhancer of Zeste Homolog 2 (EZH2) Expression on Brain Glioma Cell Proliferation and Tumorigenesis

2018 ◽  
Vol 24 ◽  
pp. 7249-7255 ◽  
Author(s):  
Tianci Cheng ◽  
Yinghui Xu
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Brain Glioma ◽  
Ezh2 Expression ◽  
Enhancer Of Zeste ◽  
Glioma Cell Proliferation

scholarly journals MiR-32 Inhibits Proliferation and Metastasis by Targeting EZH2 in Glioma

2019 ◽  
Vol 18 ◽  
pp. 153303381985413 ◽  
Author(s):  
Yuan Zhang ◽  
Jiangang Wang ◽  
Wenzhi An ◽  
Chen Chen ◽  
Wencheng Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Ectopic Expression ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Enhancer Of Zeste ◽  
Glioma Cell Proliferation ◽  
Proliferation And Metastasis ◽  
Underlying Mechanisms

Purpose: Glioma is identified as a broad category of brain and spinal cord tumors. MiR-32 is important in regulating the genesis of different cancers; however, the underlying mechanisms of miR-32 in glioma still largely unknown. This study aimed to elucidate pathobiological functions of miR-32 in glioma and verify its effect on the regulation of enhancer of zeste homolog 2. Methods: The expression of miR-32 and enhancer of zeste homolog 2 was detected by quantitative real-time polymerase chain reaction and Western blot in glioma tissues and cells. Cell Counting Kit-8 (CCK-8) assay was used to examine the effects of miR-32 on human glioma cells proliferation. Transwell assay was used to examine cell metastasis, respectively. Two bioinformatics analysis software and luciferase reporter assay were chosen to confirm targeting association between miR-32 and enhancer of zeste homolog 2. Results: MiR-32 was downregulated in glioma tissues and cells. Furthermore, enhancer of zeste homolog 2 expression was upregulated and negatively correlated with miR-32 in clinical tissues. Ectopic expression of miR-32 inhibited glioma cell proliferation, migration, and invasion. Enhancer of zeste homolog 2 was identified as direct target gene of miR-32 in glioma. Overexpression of enhancer of zeste homolog 2 ablated the inhibitory effects of miR-32. Conclusion: In summary, our finding suggests that miR-32 acts an important role in inhibiting glioma cell proliferation and metastasis and suppresses the expression of ABCC4 by directly targeting its 3′-untranslated region. The miR-32/enhancer of zeste homolog 2 axis may provide new insights to the treatment for glioma.

miR-25 promotes glioma cell proliferation by targeting CDKN1C

2015 ◽  
Vol 71 ◽  
pp. 7-14 ◽  
Author(s):  
Jihong Zhang ◽  
Xuhai Gong ◽  
Kaiyu Tian ◽  
Dongkai Chen ◽  
Jiahang Sun ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Glioma Cell Proliferation

scholarly journals NOTCH3 Is a Prognostic Factor That Promotes Glioma Cell Proliferation, Migration and Invasion via Activation of CCND1 and EGFR

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e77299 ◽  
Author(s):  
Mohammad A. Y. Alqudah ◽  
Supreet Agarwal ◽  
Maha S. Al-Keilani ◽  
Zita A. Sibenaller ◽  
Timothy C. Ryken ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Prognostic Factor ◽  
Glioma Cell ◽  
Migration And Invasion ◽  
Glioma Cell Proliferation

scholarly journals Blockage of Potassium Channel Inhibits Proliferation of Glioma Cells Via Increasing Reactive Oxygen Species

2014 ◽  
Vol 22 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Li Hu ◽  
Li-Li Li ◽  
Zhi-Guo Lin ◽  
Zhi-Chao Jiang ◽  
Hong-Xing Li ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Reactive Oxygen ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Brain Glioma ◽  
Protein Levels ◽  
Glioma Cell Proliferation

The potassium (K+) channel plays an important role in the cell cycle and proliferation of tumor cells, while its role in brain glioma cells and the signaling pathways remains unclear. We used tetraethylammonium (TEA), a nonselective antagonist of big conductance K+ channels, to block K+ channels in glioma cells, and antioxidant N-acetyl-l-cysteine (NAC) to inhibit production of intracellular reactive oxygen species (ROS). TEA showed an antiproliferation effect on C6 and U87 glioma cells in a time-dependent manner, which was accompanied by an increased intracellular ROS level. Antioxidant NAC pretreatment reversed TEA-mediated antiproliferation and restored ROS level. TEA treatment also caused significant increases in mRNA and protein levels of tumor-suppressor proteins p53 and p21, and the upregulation was attenuated by pretreatment of NAC. Our results suggest that K+ channel activity significantly contributes to brain glioma cell proliferation via increasing ROS, and it might be an upstream factor triggering the activation of the p53/p21Cip1-dependent signaling pathway, consequently leading to glioma cell cycle arrest.

Inhibition of Glioma Cell Proliferation by Neural Stem Cell Factor

2005 ◽  
Vol 74 (3) ◽  
pp. 233-239 ◽  
Author(s):  
Tsuyoshi Suzuki ◽  
Shuichi Izumoto ◽  
Kouichi Wada ◽  
Yasunori Fujimoto ◽  
Motohiko Maruno ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Neural Stem Cell ◽  
Stem Cell Factor ◽  
Glioma Cell ◽  
Glioma Cell Proliferation

scholarly journals Long Intergenic Noncoding RNA 00152 Promotes Glioma Cell Proliferation and Invasion by Interacting with MiR-16

2018 ◽  
Vol 46 (3) ◽  
pp. 1055-1064 ◽  
Author(s):  
Xin Chen ◽  
Deheng Li ◽  
Yang Gao ◽  
Wei Tang ◽  
Lao IW ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Glioma Cell ◽  
Migration And Invasion ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Glioma Cell Lines ◽  
Glioma Cell Proliferation ◽  
Proliferation And Invasion

Background/Aims: Long noncoding RNAs (lncRNAs) are a novel class of protein-noncoding transcripts that are aberrantly expressed in multiple diseases including cancers. LINC00152 has been identified as an oncogene involved in many kinds of cancer; however, its expression pattern and function in human glioma remain unclear. Methods: Quantitative real-time polymerase chain reaction was carried out to measure LINC00152 expression in human glioma cell lines and tissues. CCK-8 and EdU assays were performed to assess cell proliferation, and scratch assays and Transwell assays were used to assess cell migration and invasion, respectively. Luciferase reporter assays were carried out to determine the interaction between miR-16 and LINC00152. In vivo experiments were conducted to assess tumor formation. Results: LINC00152 was found to be significantly upregulated in human glioma cell lines and clinical samples. Knockdown of LINC00152 suppressed glioma cell proliferation, migration, and invasion in vitro. In vivo assays in nude mice confirmed that LINC00152 knockdown inhibits tumor growth. Furthermore, mechanistic investigation showed that LINC00152 binds to miR-16 in a sequence-specific manner and suppresses its expression. miR-16 inhibition strongly attenuated LINC00152 knockdown–mediated suppressive effects on proliferation, migration, and invasion. Moreover, LINC00152 induced BMI1 expression by sponging miR-16; this effect further promoted glioma cell proliferation and invasion. Conclusion: We regard LINC00152 as an oncogenic lncRNA promoting glioma cell proliferation and invasion and as a potential target for human glioma treatment.

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