Adenosine inhibits cell proliferation differently in human astrocytes and in glioblastoma cell lines

Abstract Arctigenin (ARG) is a natural lignan compound extracted from arctium lappa and has displayed anticancer functions and effective treatments in a variety of cancers.Studies had shown that Arctigenin(ARG) inhibits tumors through the AKT/MTOR pathway and mediates autophagy.However,the role in glioma cellshave not still fully understood.This study was designed to investigate whether Arctigenin(ARG) can mediateAKT/mTOR pathway in glioma to regulate autophagy,and affected glioma cells growth and survival.We found that the dose-dependent downregulation of Arctigenin(ARG),reducing cell proliferation,migration and invasion in two human glioblastoma cell lines (U87, T98G),These phenomena were reversed after the administration of the AKT agonist (SC79). Arctigenin(ARG) also affected other autophagy markers such as p62, LC3B.In addition, the apoptotic molecules cleaved-PARP,caspase-9, and cleaved-caspase3 were also dose-dependently altered.

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Smarcd1 Inhibits the Malignant Phenotypes of Human Glioblastoma Cells via Crosstalk with Notch1

Molecular Neurobiology ◽

10.1007/s12035-020-02190-z ◽

2020 ◽

Author(s):

Yihao Zhu ◽

Handong Wang ◽

Maoxing Fei ◽

Ting Tang ◽

Wenhao Niu ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Lines ◽

High Grade Glioma ◽

Glioblastoma Cell ◽

Glioblastoma Cells ◽

Human Glioblastoma ◽

Protein Levels ◽

Enhanced Expression ◽

Human Glioblastoma Cells ◽

Glioblastoma Cell Lines

AbstractSmarcd1 is a component of an evolutionary conserved chromatin remodeling complex—SWI/SNF, which is involved in transcription factor recruitment, DNA replication, recombination, and repair. Suppression of the SWI/SNF complex required for cellular differentiation and gene regulation may be inducible for cell proliferation and tumorigenicity. However, the inhibitory role of Smarcd1 in human glioblastoma cells has not been well illustrated. Both U87 and U251 human glioblastoma cell lines were employed in the present study. The lentivirus-mediated gene knockdown and overexpression approach was conducted to determine the function of Smarcd1. The protein levels were tested by western blot, and the relative mRNA contents were detected by quantitative real-time PCR. Cell viability was tested by CCK-8 and colony-forming assay. Transwell assays were utilized to evaluate the motility and invasive ability. Flow cytometry was employed to analyze cell cycle and apoptosis. SPSS software was used for statistical analysis. Low expression of Smarcd1 was observed in glioblastoma cell lines and in patients with high-grade glioma. Importantly, the depletion of Smarcd1 promoted cell proliferation, invasion, and chemoresistance, whereas enhanced expression of Smarcd1 inhibited tumor-malignant phenotypes. Mechanistic research demonstrated that overexpression of Smarcd1 decreased the expression of Notch1, while knockdown of Notch1 increased the expression of Smarcd1 through Hes1 suppression. Hence, the crosstalk between Smarcd1 and Notch1, which formed a feedback loop, was crucial in regulation of glioblastoma malignant phenotypes. Furthermore, targeting Smarcd1 could be a potential strategy for human glioblastoma treatment.

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Luteolin Decreases Epidermal Growth Factor Receptor-Mediated Cell Proliferation and Induces Apoptosis in Glioblastoma Cell Lines

Basic & Clinical Pharmacology & Toxicology ◽

10.1111/bcpt.13077 ◽

2018 ◽

Vol 123 (6) ◽

pp. 678-686 ◽

Cited By ~ 8

Author(s):

David M. Anson ◽

Rachel M. Wilcox ◽

Eric D. Huseman ◽

Trevor A. Stump ◽

Robert L. Paris ◽

...

Keyword(s):

Cell Proliferation ◽

Epidermal Growth Factor Receptor ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Cell Lines ◽

Growth Factor Receptor ◽

Glioblastoma Cell ◽

Epidermal Growth ◽

Glioblastoma Cell Lines

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miR-548x and miR-4698 controlled cell proliferation by affecting the PI3K/AKT signaling pathway in Glioblastoma cell lines

Scientific Reports ◽

10.1038/s41598-020-57588-5 ◽

2020 ◽

Vol 10 (1) ◽

Cited By ~ 3

Author(s):

Mohammad Reza kalhori ◽

Ehsan Arefian ◽

Fereshteh Fallah Atanaki ◽

Kaveh Kavousi ◽

Masoud Soleimani

Keyword(s):

Cell Proliferation ◽

Signaling Pathway ◽

Cell Lines ◽

Akt Signaling ◽

Glioblastoma Cell ◽

Akt Signaling Pathway ◽

Glioblastoma Cell Lines

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SNHG9/miR-199a-5p/Wnt2 Axis Regulates Cell Growth and Aerobic Glycolysis in Glioblastoma

Journal of Neuropathology & Experimental Neurology ◽

10.1093/jnen/nlz078 ◽

2019 ◽

Vol 78 (10) ◽

pp. 939-948 ◽

Cited By ~ 6

Author(s):

Han Zhang ◽

Danxia Qin ◽

Zhixian Jiang ◽

Jinning Zhang

Keyword(s):

Cell Proliferation ◽

Cell Growth ◽

Mrna Expression ◽

Cell Lines ◽

Aerobic Glycolysis ◽

Stress Test ◽

Glioblastoma Cell ◽

Glioblastoma Cells ◽

Qrt Pcr ◽

Glioblastoma Cell Lines

Abstract Aerobic glycolysis is a characteristic in cancers that is important for cancer cell proliferation. Emerging evidence shows that long non-coding RNA (LncRNA) participates in glucose metabolism and cell proliferation in cancer. This study explored the effect of LncRNA: SNHG9 in glioblastoma. The mRNA expression of SNHG9 in human glioma tissues and glioblastoma cell lines was measured by qRT-PCR. Glioblastoma cell lines (U87 and U251) were transfected with miR-199a-5p or SNHG9-expressing plasmid and cell viability as well as concentrations of glucose and lactate were measured. The extracellular acidification was evaluated by glycolysis stress test. The Wnt2 levels were determined by qRT-PCR and Western blot. Results showed that the mRNA expression of SNHG9 was elevated in glioblastoma tissues. The elevated SNHG9 expression was related to lower survival rate in patients with glioma. SNHG9 could downregulate miR-199a-5p and upregulate Wnt2 in glioblastoma cells. Overexpression of SNHG9 in glioblastoma cells promoted aerobic glycolysis and cell proliferation, which could be attenuated by miR-199a-5p. Results of this study indicated an effect of SNHG9/miR-199a-5p/Wnt2 axis in regulating cell growth and aerobic glycolysis in glioblastoma.

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M2 muscarinic receptors inhibit cell proliferation in human glioblastoma cell lines

Life Sciences ◽

10.1016/j.lfs.2012.04.033 ◽

2012 ◽

Vol 91 (21-22) ◽

pp. 1134-1137 ◽

Cited By ~ 16

Author(s):

M. Ferretti ◽

C. Fabbiano ◽

M. Di Bari ◽

D. Ponti ◽

A. Calogero ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Lines ◽

Muscarinic Receptors ◽

Glioblastoma Cell ◽

Human Glioblastoma ◽

Human Glioblastoma Cell ◽

M2 Muscarinic Receptors ◽

Inhibit Cell Proliferation ◽

Glioblastoma Cell Lines

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Propranolol Inhibits the Proliferation of Human Glioblastoma Cell Lines Through Notch1 and Hes1 Signaling System

10.21203/rs.3.rs-378415/v1 ◽

2021 ◽

Author(s):

Hyun Sik Kim ◽

Young Han Park ◽

Mi Jung Kwon ◽

Joon Ho Song ◽

In Bok Chang

Keyword(s):

Cell Proliferation ◽

Cell Line ◽

Cell Lines ◽

Mtt Assay ◽

Neuroblastoma Cell ◽

Neuroblastoma Cell Line ◽

Glioblastoma Cell ◽

Rt Pcr ◽

Human Glioblastoma ◽

Glioblastoma Cell Lines

Abstract PurposeThe anti-tumor effect of the beta-adrenergic receptor antagonist propranolol in breast cancer is well known; however, its activity in glioblastoma is not well-evaluated. The Notch-Hes pathway is known to regulate cell differentiation, proliferation, and apoptosis. We investigated the effect of propranolol to human glioblastoma cell lines, and the role of Notch and Hes signaling in this process.MethodsWe performed immunohistochemical staining on 31 surgically resected primary human glioblastoma tissues. We also used glioblastoma cell lines of U87-MG, LN229, and neuroblastoma cell line of SH-SY5Y in this study. The effect of propranolol and isoproterenol on cell proliferation was evaluated using the MTT assay (absorbance 570nm). The impact of propranolol on gene expression (Notch and Hes) was evaluated using real-time (RT) PCR, whereas protein levels of Notch1 and Hes1 were measured using western blotting (WB), simultaneously. Small interfering RNA (siRNA) was used to suppress the Notch gene to investigate its role in the proliferation of glioblastoma.ResultsPropranolol and isoproterenol caused a dose-dependent decrease in cell proliferation (MTT assay). RT-PCR showed an increase in Notch1 and Hes1 expression by propranolol, whereas WB demonstrated increase in Notch1 protein, but a decrease in Hes1 by propranolol. The proliferation of U87-MG and LN229 was not significantly suppressed after transfection with Notch siRNA.ConclusionThese results demonstrated that propranolol suppressed the proliferation of glioblastoma cell lines and neuroblastoma cell line, and Hes1 was more closely involved than Notch1 was in glioblastoma proliferation.

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P11.02 Hypothermia effect on glioblastoma cell viability, proliferation and migration

Neuro-Oncology ◽

10.1093/neuonc/noz126.148 ◽

2019 ◽

Vol 21 (Supplement_3) ◽

pp. iii42-iii42

Author(s):

C Fulbert ◽

C Gaude ◽

E Sulpice ◽

S Chabardès ◽

D Ratel

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Cell Lines ◽

Resection Margin ◽

Moderate Hypothermia ◽

Glioblastoma Cell ◽

Cell Proliferation And Migration ◽

And Migration ◽

Glioblastoma Cell Lines ◽

Proliferation And Migration

Abstract BACKGROUND Glioblastoma is the most common and aggressive primary brain tumor in adults. In spite of intensive treatment, patients have a poor prognosis with a median survival of 14–16 months. After surgical resection followed by postoperative chemoradiation (combined temozolomide treatment and radiotherapy), tumor recurs in the resection margin for more than 90% of patients. This recurrence results from the activation of residual glioblastoma cells beyond the resection cavity by therapy-induced injuries. To handle this issue, we propose therapeutic hypothermia as an adjuvant treatment, in order to place the resection margin in a state of hibernation. In fact, hypothermia was introduced as a promising therapeutic approach in various medical applications like cardiac arrest and pharmaco-resistant epilepsy. Only a few in vitro studies explored the effects of hypothermia on cancer cells and showed promising results. The aim of our work is to investigate the effects of hypothermia on glioblastoma cell proliferation and migration, two key cellular processes involved in cancer progression. MATERIAL AND METHODS We performed in vitro experiments on glioblastoma cell lines with different p53 status and various growth rates. For exploring the therapeutic potential of both mild and moderate hypothermia, we studied their impact on cell viability, proliferation and migration. We also performed cell cycle analysis by quantitation of DNA content using flow cytometry. RESULTS Results were similar for all glioblastoma cell lines, and demonstrated that cells were extremely sensitive to hypothermia. We showed that both mild and moderate hypothermia induced significant changes on glioblastoma cell lines behavior with a strong inhibition of cell proliferation and migration. Moderate hypothermia also affected glioblastoma cell viability and modified their distribution into the cell cycle phases. CONCLUSION Our results were comparable in all glioblastoma cell lines tested, demonstrating a consistent and universal effect of hypothermia. We showed that hypothermia significantly inhibits cell proliferation and migration, which are key processes involved in tumor growth. Proliferation arrest could be explained by the accumulation of cells in the G2/M phase of the cell cycle. Together, these results support hypothermia as a promising adjuvant therapy for glioblastoma patients. Indeed, combined with current treatments, moderate hypothermia applied at the resection margin could prevent tumor recurrence after surgical resection. There is a crucial need to propose innovative glioblastoma treatments, and hypothermia appears as a promising therapeutic way. SUPPORT This work received financial support through grants from the Groupement des Entreprises Françaises de Lutte contre le Cancer (GEFLUC Grenoble - Dauphiné - Savoie) and the Fonds de dotation Clinatec.

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