Effects of laser-induced thermotherapy (LITT) on proliferation and apoptosis of glioma cells in rat brain transplantation tumors

Objective The primary purpose of this paper is to investigate the relationship between the microRNA 146a (miR-146a) and the proliferation of cells occurring in glioblastoma multiforme. The secondary purpose of the paper is to investigate abnormalities of expression in miR-146a. Methods A real-time PCR assay was used to investigate the abnormal expression of miR-146a in glioma and adjacent tissue. Lipofection was used to transfect a mimic of miR-146a and induce the upregulation of miR-146a. Real-time PCR was used to observe the expression level of miR-146a. A cell viability analysis was conducted using MTT. A luciferase report vector was used to identify potential targets for miR-146a. Results The miR-146a component was found to be downregulated in glioma tissue compared with adjacent nontumor tissue (p<0.05). The upregulation of miR-146a in glioma cells through miR-146a mimic transfection led to reduction of cell viability and to an increase in the percentage of apoptosis. Notch1 was the name of the potential targeted gene for miR-146a in glioma. Conclusions The study found that the presence of miR-146a potentially affected the proliferation of glioma cells by regulating the rate of Notch1 expression.

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MiR-15b Targets Cyclin D1 to Regulate Proliferation and Apoptosis in Glioma Cells

BioMed Research International ◽

10.1155/2014/687826 ◽

2014 ◽

Vol 2014 ◽

pp. 1-9 ◽

Cited By ~ 29

Author(s):

Guan Sun ◽

Lei Shi ◽

Shushan Yan ◽

Zhengqiang Wan ◽

Nan Jiang ◽

...

Keyword(s):

Cell Cycle ◽

Cyclin D1 ◽

Cell Cycle Progression ◽

Therapeutic Strategy ◽

Glioma Cells ◽

Luciferase Assay ◽

Luciferase Reporter ◽

Cycle Progression ◽

Cycle Arrest ◽

Proliferation And Apoptosis

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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TGF-β1 EXPRESSION BY GLIOMA C6 CELLS IN VITRO

Experimental Oncology ◽

10.31768/2312-8852.2017.39(4):258-263 ◽

2017 ◽

Vol 39 (4) ◽

pp. 258-263 ◽

Cited By ~ 2

Author(s):

L D Liubich ◽

L M Kovalevska ◽

M I Lisyany ◽

V M Semenova ◽

T A Malysheva ◽

...

Keyword(s):

Monoclonal Antibody ◽

Rat Brain ◽

Glioma Cells ◽

C6 Glioma ◽

C6 Glioma Cells ◽

C6 Cells ◽

Fetal Rat ◽

Tgf Β1 ◽

Fetal Rat Brain

The aim of the work was to study the impact of fetal rat brain cell supernatant (FRBCS) on the expression of transforming growth factor β1 (TGF-β1) and p53 in C6 cells of rat glioma in vitro. Materials and Methods: FRBCS was obtained from suspensions of fetal rat brain cells on the 14th (E14) day of gestation. C6 glioma cells were cultured for 48 h in the presence of FRBCS or FRBCS + anti-TGF-β1 monoclonal antibody. Immunocytochemical staining for TGF-β1 and p53 was performed. Results: The proportion of TGF-β1-immunopositive tumor cells in C6 glioma cultures was statistically significantly higher than in the control cell cultures of normal fetal rat brain. FRBCS reduced the proportion of TGF-β1-immunopositive tumor cells and increased the proportion of p53-immunopositive cells in C6 glioma cultures. In cells cultured with FRBCS + anti-TGF-β1 monoclonal antibody, the above effects of FRBCS were abrogated. Conclusion: The obtained results suggest that TGF-β1 seems to be responsible for decrease in TGF-β1 expression and increase in p53 expression in C6 glioma cells treated with FRBCS.

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SPAG5 Is Involved in Human Gliomagenesis Through the Regulation of Cell Proliferation and Apoptosis

Frontiers in Oncology ◽

10.3389/fonc.2021.673780 ◽

2021 ◽

Vol 11 ◽

Author(s):

Chunhong Wang ◽

Haiyang Su ◽

Rui Cheng ◽

Hongming Ji

Keyword(s):

Cell Proliferation ◽

Cell Migration ◽

Colony Formation ◽

Glioma Cells ◽

Clinical Intervention ◽

Primary Brain Tumor ◽

The Cancer Genome Atlas ◽

Migration And Invasion ◽

Cell Migration And Invasion ◽

Proliferation And Apoptosis

BackgroundGlioma is the most frequent malignant primary brain tumor in adults.ObjectiveTo explore the role of sperm-associated antigen 5 (SPAG5) in glioma.MethodsThe association between SPAG5 expression and clinical features was investigated based on The Cancer Genome Atlas (TCGA) datasets. The function of SPAG5 in glioma was analyzed using U87 and U251 cells. Knockdown glioma cells were constructed by shRNA interference. qRT-PCR and Western blotting were used to measure the expression of SPAG5 and Cadherin 2 (CDH2). Cell proliferation and apoptosis were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, caspase 3/7 assay, and high-content screening (HCS) proliferation analysis and colony formation assay. Transwell assays and wound-healing assays were used to investigate cell migration and invasion.ResultsThe increased expression of SPAG5 was correlated with poor outcomes in glioma patients. Knocking down SPAG5 could inhibit the proliferation and colony formation and promoted the apoptosis of glioma cells. Knocking down SPAG5 could also inhibit cell migration and invasion and the expression of CDH2. Overexpression of CDH2 with SPAG5 depletion could restore the proliferation and inhibit the apoptosis of glioma cells, which also promoted cell migration and invasion.ConclusionsSPAG5 is a promising prognostic factor and potential therapeutic target for clinical intervention in glioma.

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Mir-29c Expression in Glioma and Its Effects on Tumor Cell Proliferation and Apoptosis

Iranian Journal of Public Health ◽

10.18502/ijph.v49i2.3094 ◽

2020 ◽

Author(s):

Peiquan HUI ◽

Yuling WANG ◽

Bing CHEN ◽

Zengwu WANG ◽

Shiqiang QIN

Keyword(s):

Cell Proliferation ◽

Glioma Cells ◽

Negative Control ◽

Expression Level ◽

Control Group ◽

Tumor Differentiation ◽

Blank Group ◽

Pathological Type ◽

Proliferation And Apoptosis ◽

Experimental Group

Background: To investigate the expression of microRNA-29c (miR-29c) in glioma and its effects on cell proliferation and apoptosis. Methods: A retrospective analysis was performed on 76 glioma patients in People's Hospital of Weifang, Weifang, Shandong, China from May 2013 to June 2017 (experimental group) and 63 healthy subjects in the same period (control group). qRT-PCR was used to detect the miR-29c expression. Changes of serum miR-29c expression level and the correlation of miR-29c of glioma patients with the degree of tumor differentiation and pathological type were observed. Cells were grouped before transfection into blank group (no transfection), negative control group (transfected with miRNA NC) and experimental group (transfected with miR-29c mimics). CCK-8 assay was used to detect cell proliferation, flow cytometry to detect apoptosis. Results: Expression of miR-29c in serum was significantly lower in experimental group than that in control group (P<0.05). The expression level of miR-29c of glioma patients increased with the degree of tumor differentiation (P<0.05). miR-29c in serum was not significantly correlated with the pathological type. Conclusion: miR-29c could inhibit the proliferation of glioma cells and promote apoptosis. miR-29c is lowly expressed in glioma, and the overexpression of which in glioma cells can inhibit tumor cells proliferation and promote apoptosis. It may be a tumor suppressor miRNA of glioma, and the expression level of which can be used as reference for evaluating the grade of glioma. It is indicated that the abnormal expression of miR-29c may be a key factor in the occurrence and development of glioma.

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