scholarly journals Retraction of: Effects of Fibronectin 1 on Cell Proliferation, Senescence and Apoptosis of Human Glioma Cells Through the PI3K/AKT Signaling Pathway

2020 ◽  
Vol 54 (6) ◽  
pp. 1257-1257
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Glioma Cells ◽  
Akt Signaling ◽  
Human Glioma ◽  
Akt Signaling Pathway ◽  
Human Glioma Cells

[Cell Physiol Biochem 2018;48(4):1382-1396; DOI: 10.1159/000492096]

scholarly journals Knockdown of Annexin-A1 Inhibits Growth, Migration and Invasion of Glioma Cells by Suppressing the PI3K/Akt Signaling Pathway

ASN NEURO ◽  
2021 ◽  
Vol 13 ◽  
pp. 175909142110012
Author(s):  
Liqing Wei ◽  
Li Li ◽  
Li Liu ◽  
Ru Yu ◽  
Xing Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Glioma Cell ◽  
Combined Treatment ◽  
Glioma Cells ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Akt Signaling Pathway ◽  
Down Regulation ◽  
Glioma Cell Proliferation

ANXA1, which can bind phospholipid in a calcium dependent manner, is reported to play a pivotal role in tumor progression. However, the role and mechanism of ANXA1 involved in the occurrence and development of malignant glioma are still not well studied. Therefore, we explored the effects of ANXA1 on normal astrocytes and glioma cell proliferation, apoptosis, migration and invasion and the underlying mechanisms. We found that ANXA1 was markedly up-regulated in glioma cell lines and glioma tissues. Down-regulation of ANXA1 inhibited normal astrocytes and glioma cell proliferation and induced the cell apoptosis, which suggested that the consequences of loss of Annexin 1 are not specific to the tumor cells. Furthermore, the siRNA-ANXA1 treatment significantly reduced tumor growth rate and tumor weight. Moreover, decreasing ANXA1 expression caused G2/M phase arrest by repressing expression levels of cdc25C, cdc2 and cyclin B1. Interestingly, ANXA1 did not affect the expressions of β-catenin, GSK-3β and NF-κB, the key signaling molecules associated with cancer progression. However, siRNA-ANXA1 was found to negatively regulate phosphorylation of AKT and the expression and activity of MMP2/-9. Finally, the decrease of cell proliferation and invasiveness induced by ANXA1 down-regulation was partially reversed by combined treatment with AKT agonist insulin-like growth factor-1 (IGF-1). Meanwhile, the inhibition of glioma cell proliferation and invasiveness induced by ANXA1 down-regulation was further enhanced by combined treatment with AKT inhibitor LY294002. In summary, these findings demonstrate that ANXA1 regulates proliferation, migration and invasion of glioma cells via PI3K/AKT signaling pathway.

scholarly journals Long non-coding RNA HULC regulates growth and metastasis of human glioma cells via induction of apoptosis and inhibits cell migration and invasion

2020 ◽  
Author(s):  
Junfeng Ma ◽  
Liang Zhou
Keyword(s):  
Cancer Cells ◽  
Signaling Pathway ◽  
Glioma Cells ◽  
Akt Signaling ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Human Glioma ◽  
Akt Signaling Pathway ◽  
Non Coding Rna ◽  
Long Non Coding Rna

IntroductionThe long non-coding RNA HULC has been shown to be involved in the development of several human cancers. The present study was undertaken to investigate the regulatory role of lncRNA-HULC in growth and metastasis of human glioma.Material and methodsThe gene expression of lncRNA-HULC was estimated from the clinical glioma tissues and cell lines using RT-PCR. The proliferation of transfected cancer cells was determined with the help of cell counting kit-8 (CCK8). DAPI staining and dual annexin V-FITC/PI staining procedures were used for inferring the apoptosis of transfected cancer cells. Scratch-heal and transwell chamber assays were employed for the determination of migration and invasion of transfected cells. The expression of proteins of interest was studied by western blotting technique.ResultsThe results showed that lncRNA-HULC exhibits significantly (p < 0.05) higher expression in glioma tissues and cancer cells. The knockdown of lncRNA-HULC led to a marked decline in the proliferation of glioma cells through apoptotic induction which was accompanied by upregulation of Bax and downregulation of Bcl-2. Moreover, knockdown of lncRNA-HULC significantly (p < 0.05) suppressed the migration and invasion of cancer cells in vitro. The western blot analysis showed that lncRNA-HULC exerted its effects via modulation of the PI3K/AKT signaling pathway.ConclusionsThe study revealed the possibility of targeting the PI3K/AKT signaling pathway in glioma through transcriptional knockdown of lncRNA-HULC, which might be utilized for therapeutic purposes against human glioma.

scholarly journals LRIG1 Modulated Radioresistance of Glioma via Regulating CTLA-4/AKT Signaling Pathway

2020 ◽  
Author(s):  
Shiqi Cheng ◽  
Xiangqun Huang ◽  
Raorao Yuan ◽  
Yan Zhang
Keyword(s):  
Correlation Analysis ◽  
Western Blot ◽  
Signaling Pathway ◽  
Glioma Cells ◽  
Annexin V ◽  
Akt Signaling ◽  
Potential Mechanism ◽  
Human Glioma ◽  
Akt Signaling Pathway ◽  
Glioma Tissue

Abstract Background: Radioresistance has a great impact on prognosis of glioma patients. However, the potential mechanism underlying the radioresistance of glioma cells remains largely unknown. Methods: LRIG1 overexpression model was firstly established by using Flag-LRIG1 plasmid. The expression of LRIG1, CTLA-4 proteins were detected by western blot and IHC in cells and human tissue. Real-time PCR was used for deterring mRNA expression. Cell viability and apoptosis were detected using CCK-8 and Annexin-V/propidium iodide (PI), respectively. Co-Immunoprecipitation was used for detecting the combination of LRIG1 and CTLA-4 proteins. Results: LRIG1 was significantly down-regulated in radioresistant glioma cells. Overexpressed LRIG1 could promote the radiosensitivity of glioma cells, meanwhile, inhibit the expression of p-AKT and CTLA-4 protein in radioresistant glioma cells. Furthermore, LRIG1 combined with CTLA-4 and promoted CTLA-4 degradation. In human glioma tissue, LRIG1 was down-regulated, while CTLA-4 was highly expressed in glioma tissue. Finally, correlation analysis showed that the expression of LRIG1 was negatively correlated with expression of CTLA-4 and radioresistance of glioma patients. Conclusion: Our findings demonstrated that LRIG1 facilitates radioresistance glioma cells by regulating CTLA4 /AKT signaling pathway.

Effects of AFP-activated PI3K/Akt signaling pathway on cell proliferation of liver cancer

Tumor Biology ◽  
2014 ◽  
Vol 35 (5) ◽  
pp. 4095-4099 ◽  
Author(s):  
Lu Zheng ◽  
Wei Gong ◽  
Ping Liang ◽  
XiaoBing Huang ◽  
Nan You ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway
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