scholarly journals Suppressor of fused (Sufu) represses Gli1 transcription and nuclear accumulation, inhibits glioma cell proliferation, invasion and vasculogenic mimicry, improving glioma chemo-sensitivity and prognosis

Oncotarget ◽  
2014 ◽  
Vol 5 (22) ◽  
pp. 11681-11694 ◽  
Author(s):  
Xing Liu ◽  
Xiaofeng Wang ◽  
Wenzhong Du ◽  
Lingchao Chen ◽  
Guangzhi Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Vasculogenic Mimicry ◽  
Nuclear Accumulation ◽  
Suppressor Of Fused ◽  
Glioma Cell Proliferation

scholarly journals Caveolin-1 promotes tumor cell proliferation and vasculogenic mimicry formation in human glioma

2019 ◽  
Author(s):  
Wenli Chen ◽  
Xing Cheng ◽  
Xiaobo Wang ◽  
Wenjie Hu ◽  
Jinshan Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Quantitative Polymerase Chain Reaction ◽  
Antiangiogenic Therapy ◽  
Vasculogenic Mimicry ◽  
3D Culture ◽  
Cystic Tumor ◽  
Human Glioma ◽  
Caveolin 1 ◽  
Glioma Cell Proliferation

Abstract Background: Vasculogenic mimicry (VM) plays an important role in human glioma progression and resistance to antiangiogenic therapy as a compensatory neovascularization mechanism in malignant tumors. Caveolin-1 (Cav-1) has been found to contribute to VM formation. However, it remains largely unknown whether Cav-1 expression correlates with VM in glioma. Methods: In this study, we examined CAV-1 expression levels and vasculogenic mimicry in human glioma cell lines and in 94 human gliomas with different grades and presented cox proportional hazards regression. The molecular role of Cav-1 in glioma cells was investigated using quantitative polymerase chain reaction (qRT-PCR) assays, Western blotting, CCK-8 assays, tubule formation assays. Results: Cav-1 expression and VM formation were positively correlated with each other and both are closely associated with glioma development and progression as evidenced by the presence of cystic tumor, the shortened survival time and advanced-stage glioma in glioma patients with Cav-1 overexpression/increased VM formation. Cav-1 promoted U251 glioma cell proliferation and VM formation in a Matrigel-based 3D culture model. VM-associated factors including hypoxia-inducible factor 1α (HIF-1α) and p-Akt was significantly elevated by Cav-1 overexpression but suppressed by siCav-1 in U251 cells. Conclusion: Collectively, our study identifies Cav-1 as an important regulator of glioma cell proliferation and VM formation, contributing to glioma development and progression.

scholarly journals Caveolin-1 promotes tumor cell proliferation and vasculogenic mimicry formation in human glioma

2019 ◽  
Author(s):  
Wenli Chen ◽  
Xing Cheng ◽  
Xiaobo Wang ◽  
Wenjie Hu ◽  
Jinshan Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Periodic Acid ◽  
Antiangiogenic Therapy ◽  
Vasculogenic Mimicry ◽  
3D Culture ◽  
Cystic Tumor ◽  
Human Glioma ◽  
Caveolin 1 ◽  
Glioma Cell Proliferation

Abstract Background: Vasculogenic mimicry (VM) plays an important role in human glioma progression and resistance to antiangiogenic therapy as a compensatory neovascularization mechanism in malignant tumors. Caveolin-1 (Cav-1) has been found to contribute to VM formation. However, it remains largely unknown whether Cav-1 expression correlates with VM in glioma. Methods: In this study, by performing immnunohistochemical staining of Cav-1 and CD31/Periodic acid–Schiff co-staining, we found that Cav-1 expression and VM formation were positively correlated with each other and both are closely associated with glioma development and progression as evidenced by the presence of cystic tumor, the shortened survival time and advanced-stage glioma in glioma patients with Cav-1 overexpression/increased VM formation, suggesting Cav-1 as a prognostic indicator in glioma. Results: Gain- and loss-of-function analyses showed that Cav-1 promoted U251 glioma cell proliferation and VM formation in a Matrigel-based 3D culture model. Mechanistically, overexpression of Cav-1 upregulated while knockdown of Cav-1 downregulated the mRNA/protein expression of VM-associated genes including Akt and hypoxia-inducible factor 1α (HIF-1α), respectively, suggesting that the Akt signaling and HIF-1α may be involved in Cav-1-induced glioma cell proliferation and VM formation. Conclusion: Collectively, our study identifies Cav-1 as an important regulator of glioma cell proliferation and VM formation, contributing to glioma development and progression.

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

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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