EEF1D Promotes Glioma Proliferation, Migration, and Invasion through EMT and PI3K/Akt Pathway

Xie, Congying; Zhou, Mingfeng; Lin, Jie; Wu, Zhi‐Yong; Ding, Shilei; Luo, Jie; Zhan, Zhengming; Cai, Yonghua; Xue, Shuaishuai; Song, Ye

doi:10.1155/2020/7804706

Cited by 19 publications

(16 citation statements)

References 36 publications

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“…In a study of gliomas, it was found that after knocking out EEF1D in glioma cells, the expression of mesenchymal markers including N-cadherin and snail was significantly down-regulated. In addition, β-catenin, a key transcription factor in the EMT process, was also reduced (32). These findings indicate that EEF1D is closely related to the regulation of the EMT process in glioma cells.…”

Section: The Role Of Eef1d In Tumor Invasionmentioning

confidence: 67%

“…These findings indicate that EEF1D may enhance the Akt-mTOR and Akt-Bad signaling pathways, and plays an important role in the growth of osteosarcoma cells (31). In gliomas, it has also been found that the down-regulation of EEF1D expression can inhibit the activation of the PI3K/Akt pathway and hinder cell proliferation (32).…”

Section: Eef1d Regulates Tumor Cell Proliferation and Tumor Growthmentioning

confidence: 80%

“…However, it has been found that EEF1D can inhibit the EMT process in oral squamous cell carcinoma, which suggests that the processes of cell proliferation and migration may not be coupled. On the other hand, it also suggests that the varying effects of EEF1D on the EMT process in different tumors may be due to differing tumor sources or other factors, although this mechanism needs to be further explored (32).…”

Section: The Role Of Eef1d In Tumor Invasionmentioning

confidence: 99%

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The role of EEF1D in disease pathogenesis: a narrative review

Xu¹,

Yu²,

Peng³

et al. 2021

Ann Transl Med

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Objective: The purpose of this paper was to investigate the role and mechanism of EEF1D in various diseases, especially in tumorigenesis and development, and explore the possibility of EEF1D as a biological target.Background: EEF1D is a part of the EEF1 protein complex, which can produce four protein isoforms, of which three short isoforms are used as translation elongation factors. The three short isoforms play a role in anti-aging, regulating the cell cycle, and promoting the occurrence and development of malignant tumors, and the only long-form isoform plays a role in the development of the nervous system.Methods: We searched the PubMed and Web of Science databases for literature up to January 2021 using relevant keywords, including "EEF1D", "eukaryotic translation elongation factor 1 delta", "translation elongation factor", "translation elongation factor and cancer", and "translation elongation factor and nervous system disease". We then created an overview of the literature and summarized the results of the paper.Conclusions: Through the review of relevant articles, we found that EEF1D is obviously overexpressed in a variety of tumors, and can regulate the proliferation of tumor cells and tumor growth, as well as play a role in tumor invasion. EEF1D is likely to become a new biological target for tumor therapy and diagnosis.

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Section: The Role Of Eef1d In Tumor Invasionmentioning

confidence: 67%

Section: Eef1d Regulates Tumor Cell Proliferation and Tumor Growthmentioning

confidence: 80%

Section: The Role Of Eef1d In Tumor Invasionmentioning

confidence: 99%

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The role of EEF1D in disease pathogenesis: a narrative review

Xu¹,

Yu²,

Peng³

et al. 2021

Ann Transl Med

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“…These proteins can promote the PI3K pathway. [24][25][26] Additionally, microarray data showed an increase in Akt expression with GV1001 treatment. After activation, NSCs differentiate into neural cells that replace damaged cells during neurogenesis.…”

Section: Discussionmentioning

confidence: 94%

Neuroprotective Effects of GV1001 in Animal Stroke Model and Neural Cells Subject to Oxygen-Glucose Deprivation/Reperfusion Injury

et al. 2021

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Background and Purpose Previous studies have revealed the diverse neuroprotective effects of GV1001. In this study, we investigated the effects of GV1001 on focal cerebral ischemia-reperfusion injury (IRI) in rats and oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury in neural stem cells (NSCs) and cortical neurons. Methods Focal cerebral IRI was induced by transient middle cerebral artery occlusion (MCAO). Brain diffusion-weighted imaging (DWI) was performed 2 hours after occlusion, and a total of 37 rats were treated by reperfusion with GV1001 or saline 2 hours after occlusion. Fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging, immunohistochemistry, and neurobehavioral function analyses were performed. Additionally, OGD/R-injured NSCs and cortical neurons were treated with different GV1001 concentrations. Cell viability, proliferation, migration, and oxidative stress were determined by diverse molecular analyses. Results In the stroke model, GV1001 protected neural cells against IRI. The most effective dose of GV1001 was 60 μM/kg. The infarct volume on FLAIR 48 hours after MCAO compared to lesion volume on DWI showed a significantly smaller ratio in the GV1001-treated group. GV1001-treated rats exhibited better behavioral functions than the saline-treated rats. Treatment with GV1001 increased the viability, proliferation, and migration of the OGD/R-injured NSCs. Free radicals were significantly restored by treatment with GV1001. These neuroprotective effects of GV1001 have also been demonstrated in OGD/R-injured cortical neurons. Conclusions The results suggest that GV1001 has neuroprotective effects against IRI in NSCs, cortical neurons, and the rat brain. These effects are mediated through the induction of cellular proliferation, mitochondrial stabilization, and anti-apoptotic, anti-aging, and antioxidant effects.

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“…Among these targets, eukaryotic translation elongation factor 1 delta (EEF1D) has been reported to modulate proliferation and epithelial-mesenchymal transition in oral squamous cell carcinoma [ 30 ] and promote glioma proliferation, migration, and invasion through epithelial-mesenchymal transition and PI3K/Akt pathway [ 31 ]. For eukaryotic translation initiation factor 3, subunit B (EIF3B) expression was found to be upregulated in gastric cancer tissues; it is strongly associated with proliferating cell nuclear antigen (PCNA) expression and is associated with poor outcomes in gastric cancer patients [ 32 ].…”

Section: Resultsmentioning

confidence: 99%

Downregulation of Methionine Cycle Genes MAT1A and GNMT Enriches Protein-Associated Translation Process and Worsens Hepatocellular Carcinoma Prognosis

Chen

Tsai

Huang

et al. 2022

IJMS

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The major biological methyl donor, S-adenosylmethionine (adoMet) synthesis occurs mainly in the liver. Methionine adenosyltransferase 1A (MAT1A) and glycine N-methyltransferase (GNMT) are two key enzymes involved in the functional implications of that variation. We collected 42 RNA-seq data from paired hepatocellular carcinoma (HCC) and its adjacent normal liver tissue from the Cancer Genome Atlas (TCGA). There was no mutation found in MAT1A or GNMT RNA in the 42 HCC patients. The 11,799 genes were annotated in the RNA-Seq data, and their expression levels were used to investigate the phenotypes of low MAT1A and low GNMT by Gene Set Enrichment Analysis (GSEA). The REACTOME_TRANSLATION gene set was enriched and visualized in a heatmap along with corresponding differences in gene expression between low MAT1A versus high MAT1A and low GNMT versus high GNMT. We identified 43 genes of the REACTOME_TRANSLATION gene set that are powerful prognosis factors in HCC. The significantly predicted genes were referred into eukaryotic translation initiation (EIF3B, EIF3K), eukaryotic translation elongation (EEF1D), and ribosomal proteins (RPs). Cell models expressing various MAT1A and GNMT proved that simultaneous restoring the expression of MAT1A and GNMT decreased cell proliferation, invasion, as well as the REACTOME_TRANSLATION gene EEF1D, consistent with a better prognosis in human HCC. We demonstrated new findings that downregulation or defect in MAT1A and GNMT genes can enrich the protein-associated translation process that may account for poor HCC prognosis. This is the first study demonstrated that MAT1A and GNMT, the 2 key enzymes involved in methionine cycle, could attenuate the function of ribosome translation. We propose a potential novel mechanism by which the diminished GNMT and MAT1A expression may confer poor prognosis for HCC.

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EEF1D Promotes Glioma Proliferation, Migration, and Invasion through EMT and PI3K/Akt Pathway

Cited by 19 publications

References 36 publications

The role of EEF1D in disease pathogenesis: a narrative review

The role of EEF1D in disease pathogenesis: a narrative review

Neuroprotective Effects of GV1001 in Animal Stroke Model and Neural Cells Subject to Oxygen-Glucose Deprivation/Reperfusion Injury

Downregulation of Methionine Cycle Genes MAT1A and GNMT Enriches Protein-Associated Translation Process and Worsens Hepatocellular Carcinoma Prognosis

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