scholarly journals Lnc-THOR silencing inhibits human glioma cell survival by activating MAGEA6-AMPK signaling

2019 ◽  
Vol 10 (11) ◽  
Author(s):  
Jun Xue ◽  
Shan Zhong ◽  
Bo-min Sun ◽  
Qing-Fang Sun ◽  
Liang-Yun Hu ◽  
...  
Keyword(s):  
Cell Survival ◽  
Cell Apoptosis ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Normal Brain ◽  
Human Glioma ◽  
Cell Growth And Migration ◽  
Ampk Signaling ◽  
Human Glioma Cell ◽  
Dominant Negative Mutation

AbstractLong non-coding RNA THOR (Lnc-THOR) binds to IGF2BP1, essential for its function. We here show that Lnc-THOR is expressed in human glioma tissues and cells. Its expression is extremely low or even undetected in normal brain tissues, as well as in human neuronal cells and astrocytes. We show that Lnc-THOR directly binds to IGF2BP1 in established and primary human glioma cells. shRNA-mediated Lnc-THOR knockdown or CRISPR/Cas9-induced Lnc-THOR knockout potently inhibited cell survival and proliferation, while provoking glioma cell apoptosis. Contrarily, forced overexpression of Lnc-THOR promoted glioma cell growth and migration. Importantly, Lnc-THOR shRNA or knockout activated MAGEA6-AMPK signaling in glioma cells. AMPK inactivation, by AMPKα1 shRNA, knockout, or dominant-negative mutation (T172A), attenuated Lnc-THOR shRNA-induced A172 glioma cell apoptosis. Moreover, CRISPR/Cas9-induced IGF2BP1 knockout activated MAGEA6-AMPK signaling as well, causing A172 glioma cell apoptosis. Significantly, Lnc-THOR shRNA was ineffective in IGF2BP1 KO A172 cells. In vivo, Lnc-THOR silencing or knockout potently inhibited subcutaneous A172 xenograft tumor growth in mice. MAGEA6 downregulation and AMPK activation were detected in Lnc-THOR-silenced/-KO A172 tumor tissues. Taken together, Lnc-THOR depletion inhibits human glioma cell survival possibly by activating MAGEA6-AMPK signaling.

scholarly journals Glioma cells on the run – the migratory transcriptome of 10 human glioma cell lines

BMC Genomics ◽  
2008 ◽  
Vol 9 (1) ◽  
pp. 54 ◽  
Author(s):  
Tim Demuth ◽  
Jessica L Rennert ◽  
Dominique B Hoelzinger ◽  
Linsey B Reavie ◽  
Mitsutoshi Nakada ◽  
...  
Keyword(s):  
Cell Lines ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Glioma Cell Lines

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 Regulation of human glioma cell apoptosis and invasion by miR-152-3p through targeting DNMT1 and regulating NF2

2017 ◽  
Vol 36 (1) ◽  
Author(s):  
Jin Sun ◽  
Xinhua Tian ◽  
Junqing Zhang ◽  
Yanlin Huang ◽  
Xiaoning Lin ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Glioma Cell ◽  
Human Glioma ◽  
Human Glioma Cell

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.

MAGEA6 promotes human glioma cell survival via targeting AMPKα1

2018 ◽  
Vol 412 ◽  
pp. 21-29 ◽  
Author(s):  
Si-Jian Pan ◽  
Jie Ren ◽  
Hong Jiang ◽  
Wei Liu ◽  
Liang-Yun Hu ◽  
...  
Keyword(s):  
Cell Survival ◽  
Glioma Cell ◽  
Human Glioma ◽  
Human Glioma Cell

Effect of TWIST1 Gene on the Proliferation and Apoptosis of Human Glioma Cell Line TJ861 by Regulating Mammalian Target of Rapamycin Signaling Pathway

2021 ◽  
Vol 11 (4) ◽  
pp. 580-585
Author(s):  
Fei Chen ◽  
Jiajia Hua ◽  
HongWei Shen ◽  
HongLiang Wang
Keyword(s):  
Protein Expression ◽  
Cell Line ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Glioma Cell Line ◽  
Control Group ◽  
Human Glioma ◽  
Human Glioma Cell Line ◽  
Human Glioma Cell ◽  
Mtor Protein

To observe TWIST1 gene expression in human glioma and study the effect human glioma cell line TJ861 on the proliferation and apoptosis, and further explore its potential mechanism to provide some reference for the targeted treatment of glioma in the future. Detection of cancer tissue (Carcinoma tissue) in 55 patients with glioma by RT-PCR and Expression level of TWIST1 in normal and paracancerous tissues (Adjacent tissue), the human glioma cell line TJ861 was further divided into, Nonsense sequence group, (si-NS group), TWIST1 Inhibition group (si-TWIST1 group) and control group. The glioma cells of si-NS group and si-TWIST1 group were transfected with nonsense sequence and TWIST1 siRNA respectively by liposome transfection technology. Use CCK8 assay to test the cell proliferation ability of each group at 0, 12, 24, 36, 48 and 72 hours; 48 hours after siRNA transfection, The ability of DNA replication in each group was detected by EdU staining; Apoptosis related protein expression, in each group, was analyzed by Western blot; TUNEL staining was used to test the apoptosis rate of each group; In the end, We studied TWIST1 effect knocking down on mTOR protein expression in human glioma cells and mTOR protein expression in cancer and adjacent tissues. TWIST1 expression in glioma cells was higher, compared with normal tissues (P <0.05); After transfection of TWIST1 siRNA into human glioma cell line TJ861 in vitro, CCK8 showed glioma cells proliferation ability in si-TWIST1 group at 12, 24, 36, 48 and 72 hours was lower, compared with the control group (P <0.05); After siRNA transfection at 48 hours, the DNA replication ability of glioma cells decreased significantly (P <0.05) with EdU staining; The inhibition of TWIST1 increased Bax expression in glioma cells, and inhibited Bcl-2 expression (P < 0.05) with Western blot; TUNEL staining further confirmed that the apoptosis level of glioma cells in the si-TWIST1 group was higher, compared with the control group (P <0.05). Finally, we found that mTOR protein expression in glioma was higher, compared with adjacent tissues. in vitro experiments showed that mTOR expression in glioma cells was decreased after the inhibition of TWIST1 (P <0.05). TWIST1 expression level in glioma was increased. The inhibition of TWIST1 inhibits the proliferation of glioma by blocking the mTOR signal pathway, and promote the apoptosis of glioma.

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