scholarly journals IL-17A promotes cell migration and invasion of glioblastoma cells via activation of PI3K/AKT signalling pathway

2018 ◽  
Vol 23 (1) ◽  
pp. 357-369 ◽  
Author(s):  
Qianqian Zheng ◽  
Shuo Diao ◽  
Qi Wang ◽  
Chen Zhu ◽  
Xun Sun ◽  
...  
Keyword(s):  
Cell Migration ◽  
Signalling Pathway ◽  
Migration And Invasion ◽  
Glioblastoma Cells ◽  
Cell Migration And Invasion

scholarly journals BMAL1 Suppresses Proliferation, Migration, and Invasion of U87MG Cells by Downregulating Cyclin B1, Phospho-AKT, and Metalloproteinase-9

2020 ◽  
Vol 21 (7) ◽  
pp. 2352 ◽  
Author(s):  
Do hyeong Gwon ◽  
Woo-Yong Lee ◽  
Nara Shin ◽  
Song I Kim ◽  
Kuhee Jeong ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Ectopic Expression ◽  
B Cell Lymphoma ◽  
Cyclin B1 ◽  
Migration And Invasion ◽  
Glioblastoma Cells ◽  
Gain Of Function ◽  
Cell Migration And Invasion ◽  
Phosphorylated Akt

Several studies have shown that brain and muscle aryl hydrocarbon receptor nuclear translocator-like 1 (BMAL1), an important molecule for maintaining circadian rhythms, inhibits the growth and metastasis of tumor cells in several types of cancer, including lung, colon, and breast cancer. However, its role in glioblastoma has not yet been established. Here, we addressed the function of BMAL1 in U87MG glioblastoma cells with two approaches—loss and gain of function. In the loss of function experiments, cell proliferation in U87MG cells transfected with small interfering RNA (siRNA) targeting BMAL1 was increased by approximately 24% (small interfering (si)-NC 0.91 ± 0.00 vs. si-BMAL1 1.129 ± 0.08) via upregulation of cyclin B1. In addition, cell migration and invasion of BMAL1 siRNA-treated glioblastoma cells were elevated by approximately 20% (si-NC 51.00 ± 1.53 vs. si-BMAL161.33 ± 0.88) and 209% (si-NC 21.28 ± 1.37 vs. si-BMAL1 44.47 ± 3.48), respectively, through the accumulation of phosphorylated-AKT (p-AKT) and matrix metalloproteinase (MMP)-9. Gain of function experiments revealed that adenovirus-mediated ectopic expression of BMAL1 in U87MG cells resulted in a 19% (Adenovirus (Ad)-vector 0.94± 0.03 vs. Ad-BMAL1 0.76 ± 0.03) decrease in cell proliferation compared with the control via downregulation of cyclin B1 and increased early and late apoptosis due to changes in the levels of BCL2-associated X protein (BAX), B-cell lymphoma 2 (BCL-2), and cleaved caspase-3. Likewise, cell migration and invasion were attenuated by approximately 24% (Ad-vector 55.00 ± 0.00 vs. Ad-BMAL1 41.83 ± 2.90) and 49% (Ad-vector 70.01 ± 1.24 vs. Ad-BMAL1 35.55 ± 1.78), respectively, in BMAL1-overexpressing U87MG cells following downregulation of p-AKT and MMP-9. Taken together, our results suggest that BMAL1 acts as an anti-cancer gene by altering the proliferation, migration, and invasion of glioblastoma cells. Therefore, the BMAL1 gene could be a potential therapeutic target in the treatment of glioblastoma.

scholarly journals miRNA Expression Profiling in Migrating Glioblastoma Cells: Regulation of Cell Migration and Invasion by miR-23b via Targeting of Pyk2

PLoS ONE ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. e39818 ◽  
Author(s):  
Joseph C. Loftus ◽  
Julianna T. D. Ross ◽  
Kimberly M. Paquette ◽  
Vincent M. Paulino ◽  
Sara Nasser ◽  
...  
Keyword(s):  
Cell Migration ◽  
Mirna Expression ◽  
Expression Profiling ◽  
Migration And Invasion ◽  
Glioblastoma Cells ◽  
Cell Migration And Invasion ◽  
Mirna Expression Profiling

scholarly journals Betulin terpenoid targets OVCAR-3 human ovarian carcinoma cells by inducing mitochondrial mediated apoptosis, G2/M phase cell cycle arrest, inhibition of cell migration and invasion and modulating mTOR/PI3K/AKT signalling pathway

2021 ◽  
Vol 67 (2) ◽  
pp. 14-19
Author(s):  
Qin Yang ◽  
Zhiyi Fei ◽  
Chunyan Huang
Keyword(s):  
Cell Cycle ◽  
Cell Migration ◽  
Carcinoma Cells ◽  
Signalling Pathway ◽  
Phase Cell ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Cycle Arrest ◽  
Anticancer Effects ◽  
M Phase

The main purpose of the current research work was to study in vitro anticancer effects of betulin in OVCAR-3 human ovarian carcinoma cells along with examining its effects on cellular apoptosis, cell cycle phase distribution, cell migration and invasion and mTOR/PI3K/AKT signalling pathway. The cell proliferation of OVCAR-3 cells at various doses of the drug was studied by CCK8 cell viability assay. Effects on cell apoptosis were studied by fluorescence microscopy and western blot. Effects on cell cycle were evaluated by flow cytometry and western blot. Transwell assays were used to study effects on cell migration and invasion. The results indicated that betulin led to significant reduction of OVCAR-3 cell viability in a dose-dependent as well as time dependent manner. Betulin also led to reduction in cell colonies. The anticancer effects of betulin were due to the induction of apoptosis which was seen by increased apoptotic cells with yellow and orange fluorescence. Betulin prompted mitochondrial apoptosis which was also associated with alteration in the apoptosis-related protein expression (Bax, Bad and Bcl-2 and Bcl-xL). The molecule also led to G2/M phase cell cycle arrest on OVACR-3 ovarian carcinoma cells. It was also observed that betulin could inhibit the migration and invasion of the ovarian cancer cells in a concentration-dependent manner. Betulin molecule also resulted in blocking of mTOR/PI3K/AKT signalling pathway.  In conclusion, this study clearly indicates the anticancer effects of betulin natural product in OVCAR-3 human ovarian cancer cells are mediated via apoptosis induction, G2/M phase cell cycle arrest, cell migration and invasion inhibition and targeting of mTOR/PI3K/AKT signalling pathway.

scholarly journals Anticancer effects of 7,8-dihydromethysticin in human leukemia cells are mediated via cell-cycle dysregulation, inhibition of cell migration and invasion and targeting JAK/STAT pathway

2021 ◽  
Vol 71 (4) ◽  
pp. 645-655
Author(s):  
Yi Xiao ◽  
Taoran Deng ◽  
Lijun Jiang ◽  
Di Wang
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Clonogenic Assay ◽  
Cyclin B1 ◽  
Signalling Pathway ◽  
Leukemia Cells ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Dependent Inhibition

Abstract The main focus of this research work was to study the anti-cancer properties of 7,8-dihydromethysticin against HL-60 leukemia cells. Investigations were also performed to check its impact on the phases of the cell cycle, cell migration and invasion, JAK/STAT signalling pathway and intracellular mitochondrial membrane potential (MMP) and reactive oxygen species (ROS). Cell proliferation was assessed through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay and effects on colony formation were examined via clonogenic assay. Flow cytometry and Western blott analysis were performed to investigate the distribution of cell cycle phases. Flow cytometric analysis was performed for the examination of MMP and ROS production. The effect on JAK/STAT signalling pathway was examined through Western blot analysis. Results depicted that 7,8-dihydromethysticin induced concentration- as well as time-dependent inhibition of cell proliferation in leukemia HL-60 cells. Clonogenic assay indicated potential suppression in leukemia HL-60 cell colonies. The 7,8-dihydromethysticin molecule also caused cell cycle arrest at G2/M-phase along with concentration-dependent inhibition of cyclin B1, D1 and E. ROS and MMP measurements indicated significant ROS enhancement and MMP suppression with increasing 7,8-dihydromethysticin concentrations. Additionally, 7,8-dihydromethysticin led to remarkable dose-reliant inhibition of cell invasion as well as cell migration. Therefore, 7,8-dihydromethysticin should be considered a valuable candidate for leukemia research and chemoprevention.

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