Inhibition of NF-kB activation confers sensitivity to TNFa by impairment of cell-cycle progression in human glioma cells

Aim. To investigate the role and mechanism of miR-15b in the proliferation and apoptosis of glioma.Methods. The miR-15b mimics were transfected into human glioma cells to upregulate the miR-15b expression. Cyclin D1 was determined by both western blotting analysis and luciferase reporter assay. Methylthiazol tetrazolium (MTT) and flow cytometry were employed to detect the cell proliferation, cell cycle, and apoptosis.Results. Overexpression of miR-15b inhibits proliferation by arrested cell cycle progression and induces apoptosis, possibly by directly targeting Cyclin D1. Both luciferase assay and bioinformatics search revealed a putative target site of miR-15b binding to the 3′-UTR of Cyclin D1. Moreover, expression of miR-15b in glioma tissues was found to be inversely correlated with Cyclin D1 expression. Enforced Cyclin D1 could abrogate the miR-15b-mediated cell cycle arrest and apoptosis.Conclusions. Our findings identified that miR-15b may function as a glioma suppressor by targeting the Cyclin D1, which may provide a novel therapeutic strategy for treatment of glioma.

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Induction of G1 Cell Cycle Arrest in Human Glioma Cells by Salinomycin Through Triggering ROS-Mediated DNA Damage In Vitro and In Vivo

Neurochemical Research ◽

10.1007/s11064-016-2132-5 ◽

2016 ◽

Vol 42 (4) ◽

pp. 997-1005 ◽

Cited By ~ 14

Author(s):

Shi-Jun Zhao ◽

Xian-Jun Wang ◽

Qing-Jian Wu ◽

Chao Liu ◽

Da-Wei Li ◽

...

Keyword(s):

Cell Cycle ◽

Dna Damage ◽

Cell Cycle Arrest ◽

Glioma Cells ◽

Human Glioma ◽

Human Glioma Cells ◽

Cycle Arrest ◽

G1 Cell Cycle Arrest

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Apoptosis related to telomere instability and cell cycle alterations in human glioma cells treated by new highly selective G-quadruplex ligands

Oncogene ◽

10.1038/sj.onc.1208468 ◽

2005 ◽

Vol 24 (18) ◽

pp. 2917-2928 ◽

Cited By ~ 164

Author(s):

Gaëlle Pennarun ◽

Christine Granotier ◽

Laurent R Gauthier ◽

Dennis Gomez ◽

Françoise Hoffschir ◽

...

Keyword(s):

Cell Cycle ◽

Glioma Cells ◽

Human Glioma ◽

Human Glioma Cells ◽

G Quadruplex ◽

Cell Cycle Alterations

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Silencing myelin protein zero-like 1 expression suppresses cell proliferation and invasiveness of human glioma cells by inhibiting multiple cancer-associated signal pathways

Journal of Neurorestoratology ◽

10.26599/jnr.2021.9040017 ◽

2021 ◽

Vol 9 (4) ◽

pp. 229-244

Author(s):

Simiao Zhang ◽

Sandian Zhang ◽

Hongzhen Wang ◽

Xuege Huang ◽

Jinzhi Wang ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Cell Lines ◽

Colony Formation ◽

Glioma Cells ◽

Myelin Protein ◽

Human Glioma ◽

Myelin Protein Zero ◽

Human Glioma Cells ◽

Protein Zero

Glioma is the most common primary malignant tumor of the adult central nervous system. It has high morbidity and poor survival. Myelin protein zero-like protein 1 (MPZL1) is a cell surface glycoprotein that activates numerous adhesion-dependent signaling pathways. MPZL1 plays important roles in human cancers that include metastatic process; however, it is not clear if MPZL1 plays a role in human glioma. Therefore, this study aimed to determine if silencing MPZL1 impacted the cell proliferative features of human glioma cells. First, MPZL1 expression was investigated in human glioma samples and tumor cell lines. Then the effects of small interfering RNA (siRNA)-targeting MPZL1 were analyzed on proliferation, colony formation, cell cycle progression, and invasion of human glioma cells. The results from this study demonstrated that MPZL1 was highly expressed in human glioma tissues and glioma cell lines. In addition, knockdown of MPZL1 significantly inhibited cell proliferation, colony formation, and invasiveness of glioma cells, and effectively induced cell cycle arrest at the G1 phase. Western blotting analysis indicated that silencing MPZL1 expression downregulated the expression of matrix metalloproteinase-2 (MMP-2), WNT1, caspase-3, cyclin A1, epidermal growth factor receptor (EGFR), and signal transducer and activator of transcription 3 (STAT3), and upregulated p53. The results from this study suggest that MPZL1 might be a marker for tumors and could be a potential therapeutic target for human glioma.

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