scholarly journals Cryptotanshinone inhibits human glioma cell proliferation in vitro and in vivo through SHP-2-dependent inhibition of STAT3 activation

2017 ◽  
Vol 8 (5) ◽  
pp. e2767-e2767 ◽  
Author(s):  
Liang Lu ◽  
Sulin Zhang ◽  
Cuixian Li ◽  
Chun Zhou ◽  
Dong Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Dependent Inhibition ◽  
Glioma Cell Proliferation ◽  
Proliferation In Vitro

scholarly journals MicroRNA-585 inhibits human glioma cell proliferation by directly targeting MDM2

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Wangsheng Chen ◽  
Lan Hong ◽  
Changlong Hou ◽  
Yibin Wang ◽  
Fei Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Human Glioma Cell ◽  
Glioma Cell Proliferation

Abstract Background MicroRNAs (miRNAs) are important regulators for cancer cell proliferation. miR-585 has been shown to inhibit the proliferation of several types of cancer, however, little is known about its role in human glioma cells. Methods miR-585 levels in human glioma clinical samples and cell lines were examined by quantitative real-time PCR (qRT-PCR) analysis. Cell proliferation was measured by Cell Counting Kit-8 (CCK-8) and EdU incorporation assays in vitro. For in vivo investigations, U251 cells were intracranially inoculated in BALB/c nude mice and xenografted tumors were visualized by magnetic resonance imaging (MRI). Results miR-585 expression is downregulated in human glioma tissues and cell lines compared with non-cancerous counterparts. Additionally, miR-585 overexpression inhibits and its knockdown promotes human glioma cell proliferation in vitro. Moreover, miR-585 overexpression also inhibits the growth of glioma xenografts in vivo, suggesting that miR-585 may act as a tumor suppressor to inhibit the proliferation of human glioma. Furthermore, miR-585 directly targets and decreases the expression of oncoprotein murine double minute 2 (MDM2). More importantly, the restoration of MDM2 via enforced overexpression markedly rescues miR-585 inhibitory effect on human glioma cell proliferation, thus demonstrating that targeting MDM2 is a critical mechanism by which miR-585 inhibits human glioma cell proliferation. Conclusions Our study unveils the anti-proliferative role of miR-585 in human glioma cells, and also implicates its potential application in clinical therapy.

scholarly journals Probucol suppresses human glioma cell proliferation in vitro via ROS production and LKB1-AMPK activation

2014 ◽  
Vol 35 (12) ◽  
pp. 1556-1565 ◽  
Author(s):  
Yong-sheng Jiang ◽  
Jing-an Lei ◽  
Fang Feng ◽  
Qi-ming Liang ◽  
Fu-rong Wang
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Ros Production ◽  
Ampk Activation ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Glioma Cell Proliferation ◽  
Proliferation In Vitro

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.

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 Long Noncoding RNA H19 Promotes Proliferation and Invasion in Human Glioma Cells by Downregulating miR-152

2018 ◽  
Vol 26 (9) ◽  
pp. 1419-1428 ◽  
Author(s):  
Lei Chen ◽  
Yuhai Wang ◽  
Jianqing He ◽  
Chunlei Zhang ◽  
Junhui Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Glioma Cell Lines ◽  
Glioma Cell Proliferation ◽  
Proliferation And Invasion

miR-152 and lncRNA H19 have been frequently implicated in various cellular processes including cell proliferation, invasion, angiogenesis, and apoptosis. However, the interaction between miR-152 and H19 in glioma has never been reported. RT-qPCR was used to examine the expression of miR-152 and H19 in human glioma cell lines and normal human astrocytes (NHAs). The interaction between miR-152 and lncRNA H19 was assessed by dual-luciferase reporter assay. MTT assay and Transwell invasion assay were used to determine the proliferation and invasion of U251 and U87 cells. A xenograft tumor experiment was performed to confirm the role of H19 in vivo. The results showed that H19 expression was upregulated and miR-152 expression was downregulated in human glioma cell lines. H19 downregulation or miR-152 upregulation suppressed glioma cell proliferation and invasion in vitro. Moreover, H19 and miR-152 directly regulated each other. Furthermore, decreased miR-152 expression alleviated si-H19-induced inhibitory effects on proliferation and invasion in glioma cells. As expected, H19 silencing hindered glioma growth in vivo. Taken together, H19 promoted glioma cell proliferation and invasion by negatively regulating miR-152 expression, providing evidence for the potential application of H19 as a biomarker and therapy target for glioma.

scholarly journals Interfering with hyaluronic acid metabolism suppresses glioma cell proliferation by regulating autophagy

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Tao Yan ◽  
Xin Chen ◽  
Hua Zhan ◽  
Penglei Yao ◽  
Ning Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Hyaluronic Acid ◽  
Tumor Microenvironment ◽  
Glioma Cell ◽  
Underlying Mechanism ◽  
Uridine Diphosphate ◽  
Glioma Cell Proliferation ◽  
Proliferation In Vitro

AbstractThe tumor microenvironment plays an important role in tumor progression. Hyaluronic acid (HA), an important component of the extracellular matrix in the tumor microenvironment, abnormally accumulates in a variety of tumors. However, the role of abnormal HA accumulation in glioma remains unclear. The present study indicated that HA, hyaluronic acid synthase 3 (HAS3), and a receptor of HA named CD44 were expressed at high levels in human glioma tissues and negatively correlated with the prognosis of patients with glioma. Silencing HAS3 expression or blocking CD44 inhibited glioma cell proliferation in vitro and in vivo. The underlying mechanism was attributed to the inhibition of autophagy flux and maintaining glioma cell cycle arrest in G1 phase. More importantly, 4-methylumbelliferone (4-MU), a small competitive inhibitor of Uridine diphosphate (UDP) with the ability to penetrate the blood-brain barrier (BBB), also inhibited glioma cell proliferation in vitro and in vivo. Thus, approaches that interfere with HA metabolism by altering the expression of HAS3 and CD44 and the administration of 4-MU potentially represent effective strategies for glioma treatment.

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