scholarly journals Correction to: MiR-126 Regulates the ERK Pathway via Targeting KRAS to Inhibit the Glioma Cell Proliferation and Invasion

2021 ◽  
Author(s):  
Yang Li ◽  
Yunqian Li ◽  
Pengfei Ge ◽  
Chengyuan Ma
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Erk Pathway ◽  
Glioma Cell Proliferation ◽  
Proliferation And Invasion

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 miR-6869-5p Inhibits Glioma Cell Proliferation and Invasion via Targeting PGK1

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Fakai Wang ◽  
Huanjun Zhang ◽  
Bing Liu ◽  
Wei Liu ◽  
Zengchao Zhang
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Negative Association ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Glioma Cell Proliferation ◽  
Precise Role ◽  
Proliferation And Invasion

Accumulating studies have suggested the dysregulated microRNAs (miRNAs) play important roles in brain tumors, including glioma. miR-6869-5p has been documented to be aberrantly expressed in diverse cancers. However, the precise role of miR-6869-5p in glioma remains poorly understood. This study is aimed at evaluating its modifying effects on glioma. Significantly decreased expression of miR-6869-5p was found in glioma tissues and cells. Negative association was documented between miR-6869-5p and PGK1 in glioma cells, and PGK1 was demonstrated to be a targeted gene of this miRNA by luciferase reporter assay. miR-6869-5p regulated glioma cell proliferation and invasion via targeting PGK1. In addition, the survival analysis had suggested that low miR-6869-5p expression predicted poor prognosis of glioma patients. This study has suggested that miR-6869-5p is a useful tumor suppressor and prognostic marker in glioma.

scholarly journals NLRP3 Promotes Glioma Cell Proliferation and Invasion via the Interleukin-1β/NF-κB p65 Signals

2019 ◽  
Vol 27 (5) ◽  
pp. 557-564 ◽  
Author(s):  
Liping Xue ◽  
Bin Lu ◽  
Bibo Gao ◽  
Yangyang Shi ◽  
Jingqi Xu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Glioma Cell ◽  
Inflammatory Diseases ◽  
Interleukin 1 ◽  
Malignant Gliomas ◽  
Pyrin Domain ◽  
Crucial Component ◽  
Glioma Cell Proliferation ◽  
Proliferation And Invasion

Because of the characteristics of high invasiveness, relapse, and poor prognosis, the management of malignant gliomas has always been a great challenge. Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) is a crucial component of the NLRP3 inflammasome, a multiprotein complex that can trigger caspase 1/interleukin-1 (IL-1)-mediated inflammatory response once activated and participates in the pathogeny of diverse inflammatory diseases as well as cancers. We examined the function of NLRP3 in the development of glioma. Glioma cells were treated with NLRP3 interference or overexpression vectors, recombinant IL-1β, IL-1β antibody, and NF-κB inhibitor. Cell proliferation and invasion were assessed by CCK-8 and Transwell assays. Gene expression was detected by PCR, Western blot, and ELISA. NLRP3 and NF-κB p65 increased and were positively correlated in glioma tissues. NLRP3 knockdown suppressed glioma cell growth and invasion with the decrease of IL-1β and NF-κB p65. Conversely, forced expression of NLRP3 promoted cell growth. NLRP3 silencing suppressed ectogenous IL-1β-elevated cell proliferation and invasion, whereas IL-1β elimination impaired the proproliferation effect of NLRP3 hyperexpression. Furthermore, NF-κB blockage abrogated IL-1β and NLRP3 hyperexpression increased cell growth and invasion. NLRP3 promoted the growth and invasion of gliomas via the IL-1β/NF-κB p65 signals.

miRNA-451 inhibits glioma cell proliferation and invasion by downregulating glucose transporter 1

Tumor Biology ◽  
2016 ◽  
Vol 37 (10) ◽  
pp. 13751-13761 ◽  
Author(s):  
Hongbao Guo ◽  
Yang Nan ◽  
Yingwei Zhen ◽  
Yahui Zhang ◽  
Liyun Guo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Glucose Transporter ◽  
Glucose Transporter 1 ◽  
Glioma Cell Proliferation ◽  
Proliferation And Invasion

scholarly journals miR-133b inhibits glioma cell proliferation and invasion by targeting Sirt1

Oncotarget ◽  
2016 ◽  
Vol 7 (24) ◽  
pp. 36247-36254 ◽  
Author(s):  
Chuntao Li ◽  
Zhixiong Liu ◽  
Kui Yang ◽  
Xin Chen ◽  
Yu Zeng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Glioma Cell Proliferation ◽  
Proliferation And Invasion

TAMI-45. MICROGLIAL CYTOKINES INDUCE INVASIVENESS AND PROLIFERATION THROUGH PYK2 AND FAK ACTIVATION IN HUMAN GLIOBLASTOMA CELL

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi207-vi208
Author(s):  
Rebeca Nunez ◽  
Miguel Mayol-Del Valle ◽  
Luis Almodovar ◽  
Lilia Kucheryavykh
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Glioma Cell ◽  
Expression Patterns ◽  
Critical Role ◽  
Cell Fraction ◽  
Glioma Invasion ◽  
Glioma Cell Proliferation ◽  
Proliferation And Invasion

Abstract Glioblastoma (GBM) is the most aggressive and highly invasive primary brain tumor in adults. Evidence suggests that microglia create a microenvironment favoring glioma invasion and proliferation. Indeed, previous reports indicate the involvement of focal adhesion kinase (FAK) signaling cascades in glioma cell proliferation. Besides, studies from our laboratory support a critical role of Pyk2, a relative of FAK, in glioma invasion by tumor-infiltrating microglia. However, the microglial-released factors modulating Pyk2 and FAK signaling pathways are unknown. In this study, 20 human GBM specimens were evaluated to identify the cytokine expression patterns in purified microglia and FAK and Pyk2 phosphorylation in glioma cell fraction by RT-PCR and western blot. A Pierson correlation test demonstrated a high correlation (0.8-1.0) of gene expression for PDGFα, PDGFβ, SDF-1α, IL-6, IL-8, and EGF in percoll-purified microglia, and pPyk2(Y579/580) and pFAK(Y925) levels in glioma cell fraction. The role of cytokines in cell invasion and proliferation by Pyk2/FAK activation was further investigated in primary cell lines from three patients. Thirty percent up-regulation of pPyk2 and pFAK was detected in glioma cells treated (2 hrs.) with microglia conditioned media (MCM) compared to control cells. siPyk2 or siFAK knockdown identified IL-6 (100 μM) and EGF (1 μM) as key factors of Pyk2- and FAK-dependent activation in all glioma cell lines. Similar results with siPyk2 or siFAK were observed for matrix degradation, invadopodia formation, cell viability, and mitosis. Indeed, Tocilizumab (IL-6R blocker, 100 ng/mL) and Gefitinib (EGFR blocker, 1 μM) reversed the effect of MCM on glioma cell proliferation and invasion in all cell lines evaluated. These findings support a pivotal role of Pyk2 and FAK in enhancing proliferation and invasion of glioma tumors through IL-6 and EGF-dependent pathways. The latter could be of clinical relevance for new therapeutic developments in GBM patients.

scholarly journals CBX2 Induces Glioma Cell Proliferation and Invasion Through the Akt/PI3K Pathway

2021 ◽  
Author(s):  
Le Wang ◽  
Bingcheng Ren ◽  
Yue Zhong ◽  
Yang NAN
Keyword(s):  
Cell Proliferation ◽  
Glioma Cell ◽  
Animal Experiments ◽  
Tumor Development ◽  
Pi3k Pathway ◽  
Glioma Cell Proliferation ◽  
Glioma Growth ◽  
Primary Intracranial Tumor ◽  
Proliferation And Invasion

Abstract Background Glioma is the most common primary intracranial tumor. Abnormal expression of CBX2(ChromoBox2) is associated with tumorigenesis and tumor development. Methods TCGA data in UALCAN showed that CBX2 was overexpressed in glioma tissue. To confirm the role of CBX2 in glioma, we regulated the level of CBX2 and conducted colony formation, Transwell, and CCK-8 assays to verify the effect of CBX2. Results The results showed that CBX2 knockdown reduced glioma cell proliferation and invasion and that the cells were less tumorigenic. CBX2 overexpression induced glioma cell proliferation and invasion and glioma stem cell self-renewal. The animal experiments showed that CBX2 knockdown inhibited glioma growth and improved survival time. CBX2 knockdown inhibited activation of the Akt/PI3K pathway. EGF rescued the effects of CBX2. Conclusion We hypothesized that CBX2 induced the growth and invasion of glioma cells via the Akt/PI3K pathway.

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