scholarly journals HOXA5 Is Recognized as a Prognostic-Related Biomarker and Promotes Glioma Progression Through Affecting Cell Cycle

2021 ◽  
Vol 11 ◽  
Author(s):  
Fengqin Ding ◽  
Ping Chen ◽  
Pengfei Bie ◽  
Wenhua Piao ◽  
Quan Cheng
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Glioma Cell ◽  
Molecular Subtype ◽  
High Grade Glioma ◽  
Surgical Removal ◽  
Data Set ◽  
M Phase ◽  
Glioma Cell Proliferation ◽  
Glioma Progression

Glioma is malignant tumor derives from glial cells in the central nervous system. High-grade glioma shows aggressive growth pattern, and conventional treatments, such as surgical removal and chemo-radiotherapy, archive limitation in the interference of this process. In this work, HOXA5, from the HOX family, was identified as a glioma cell proliferation-associated factor by investigating its feature in the TCGA and CGGA data set. High HOXA5 expression samples contain unfavorable clinical features of glioma, including IDH wild type, un-methylated MGMT status, non-codeletion 1p19q status, malignant molecular subtype. Survival analysis indicates that high HOXA5 expression samples are associated with worse clinical outcome. The CNVs and SNPs profile difference further confirmed the enrichment of glioma aggressive related biomarkers. In the meantime, the activation of DNA damage repair-related pathways and TP53-related pathways is also related to HOXA5 expression. In cell lines, U87MG and U251, by interfering HOXA5 expression significantly inhibit glioma progression and apoptosis, and cell cycle is arrested at the G2/M phase. Collectively, increased HOXA5 expression can promote glioma progression via affecting glioma cell proliferation.

Effect and mechanism of YB-1 knockdown on glioma cell growth, migration, and apoptosis

2020 ◽  
Vol 52 (2) ◽  
pp. 168-179 ◽  
Author(s):  
Huilin Gong ◽  
Shan Gao ◽  
Chenghuan Yu ◽  
Meihe Li ◽  
Ping Liu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Glioma Cell ◽  
Cell Transformation ◽  
Malignant Cell ◽  
Protein Levels ◽  
Glioma Progression

Abstract Y-box binding protein 1 (YB-1) is manifested as its involvement in cell proliferation and differentiation and malignant cell transformation. Overexpression of YB-1 is associated with glioma progression and patient survival. The aim of this study is to investigate the influence of YB-1 knockdown on glioma cell progression and reveal the mechanisms of YB-1 knockdown on glioma cell growth, migration, and apoptosis. It was found that the knockdown of YB-1 decreased the mRNA and protein levels of YB-1 in U251 glioma cells. The knockdown of YB-1 significantly inhibited cell proliferation, colony formation, and migration in vitro and tumor growth in vivo. Proteome and phosphoproteome data revealed that YB-1 is involved in glioma progression through regulating the expression and phosphorylation of major proteins involved in cell cycle, adhesion, and apoptosis. The main regulated proteins included CCNB1, CCNDBP1, CDK2, CDK3, ADGRG1, CDH-2, MMP14, AIFM1, HO-1, and BAX. Furthermore, it was also found that YB-1 knockdown is associated with the hypo-phosphorylation of ErbB, mTOR, HIF-1, cGMP-PKG, and insulin signaling pathways, and proteoglycans in cancer. Our findings indicated that YB-1 plays a key role in glioma progression in multiple ways, including regulating the expression and phosphorylation of major proteins associated with cell cycle, adhesion, and apoptosis.

Forced FoxO1:S249V expression suppressed glioma cell proliferation through G2/M cell cycle arrests and increased apoptosis

2018 ◽  
Vol 41 (2) ◽  
pp. 189-198 ◽  
Author(s):  
Xiang-yu Piao ◽  
Wenzhe Li ◽  
Zhi Li ◽  
Nianzhu Zhang ◽  
Hui Fang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Glioma Cell ◽  
M Cell ◽  
Glioma Cell Proliferation

MicroRNA-370-3p inhibits human glioma cell proliferation and induces cell cycle arrest by directly targeting β-catenin

2016 ◽  
Vol 1644 ◽  
pp. 53-61 ◽  
Author(s):  
Zesheng Peng ◽  
Tingfeng Wu ◽  
Yuntao Li ◽  
Zhou Xu ◽  
Shenqi Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Glioma Cell ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Cycle Arrest ◽  
Glioma Cell Proliferation

Knockdown of HOXC6 inhibits glioma cell proliferation and induces cell cycle arrest by targeting WIF-1 in vitro and vivo

2018 ◽  
Vol 214 (11) ◽  
pp. 1818-1824 ◽  
Author(s):  
Teng-feng Yan ◽  
Miao-jing Wu ◽  
Bing Xiao ◽  
Qing Hu ◽  
Yang-Hua Fan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Glioma Cell ◽  
Cycle Arrest ◽  
Glioma Cell Proliferation

scholarly journals MiRNAs Mediate GDNF-Induced Proliferation and Migration of Glioma Cells

2017 ◽  
Vol 44 (5) ◽  
pp. 1923-1938 ◽  
Author(s):  
Bao-Le Zhang ◽  
Fu-Lu Dong ◽  
Ting-Wen Guo ◽  
Xiao-He Gu ◽  
Lin-Yan Huang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Adhesion ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Cell Proliferation And Migration ◽  
Differentially Expressed Mirnas ◽  
Glioma Cell Proliferation ◽  
And Migration ◽  
Proliferation And Migration

Background/Aims: Glial cell line-derived neurotrophic factor (GDNF) is an important factor promoting invasive glioma growth. This study was performed to reveal a unique mechanism of glioma cell proliferation and migration. Methods: Human U251 glioma cells were used to screen the optimal GDNF concentration and treatment time to stimulate proliferation and migration. MicroRNA (MiRNA) expression profiles were detected by microarray and confirmed by real-time polymerase chain reaction (PCR). The target genes of differentially expressed miRNAs were predicted by miRWalk, and those targeted by multiple miRNAs were screened with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. A regulatory miRNA network was constructed using ingenuity pathway analysis (IPA). Target gene expression of differentially expressed miRNAs was examined by real-time PCR or mRNA microarray. Results: The results show that 50 ng/mL GDNF for 24 h significantly promotes U251 glioma cell proliferation and migration (P < 0.05). Seven miRNAs (hsa-miR-194-5p, hsa-miR-152-3p, hsa-miR-205-5p, hsa-miR-629-5p, hsa-miR-3609, hsa-miR-183-5p, and hsa-miR-487b-3p) were significantly up-regulated after GDNF treatment (P < 0.05). These miRNAs are primarily involved in signal transduction, cell adhesion and cell cycle through mitogen-activated protein kinase (MAPK) signaling, focal adhesion and glioma signal pathways. Five of these miRNAs (hsa-miR-194-5p, hsa-miR-152-3p, hsa-miR-205-5p, hsa-miR-183-5p, and hsa-miR-487b-3p) co-regulate TP53 and Akt. mRNA expression levels of four genes co-targeted by two or more up-regulated miRNAs were significantly decreased after GDNF treatment (P < 0.05). Conclusion: GDNF treatment of U251 glioma cells significantly increased the expression of seven miRNAs involved in cell adhesion and the cell cycle.

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