High expression of eIF3d is associated with poor prognosis in patients with gastric cancer

He, Jiaqi; Wang, Xuefei; Cai, Jingyi; Wang, Wei; Qin, Xinyu

doi:10.2147/cmar.s142324

Cited by 18 publications

(14 citation statements)

References 24 publications

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“…We then sought to determine whether eIF3d affects the function of CD8+ T cells. Previous studies on eIF3d in tumours have shown that over expression leads to the abnormal proliferation of tumour cells [35, 41, 43]. Our study demonstrated that a reduction in eIF3d expression in human CD8+ T cells attenuated cell proliferation and secretion of IFN-γ and promoted apoptosis, which was consistent with the finding of the function of this protein in tumour cells.…”

Section: Discussionsupporting

confidence: 91%

“…We first systematically analysed the expression levels of 13 eIF3 subunit mRNAs in EHI and HCs and found that expression of eIF3d mRNA was lowest in the RP group and significantly negatively correlated with disease progression. Previous reports have indicated that eIF3d can serve as a marker for tumour metastasis and prognosis [24, 41, 42]. Our study suggests that in EHI, a low level of eIF3d in the host is correlated with rapid disease progression.…”

Section: Discussionsupporting

confidence: 66%

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Reduced eIF3d accelerates HIV disease progression by attenuating CD8+ T cell function

et al. 2019

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Background In human immunodeficiency virus (HIV) infection, 10–15% of individuals exhibit a rapid decline in CD4+ T cells and become rapid progressors (RPs). Overall, understanding the factors affecting rapid disease progression in early HIV infection (EHI) can aid in treatment initiation. Recent studies show that eIF3s, classic scaffold proteins during the translation initiation process, can directly promote or inhibit the translation of mRNA, therefore participating in the regulation of cell function. However, to our knowledge, it has not been addressed whether eIF3s are involved in the diverse prognosis of HIV infection. Methods Expression of eIF3s in primary cells from early or chronic HIV-infected patients was detected by real-time PCR. To investigate the potential mechanisms of eIF3d in the regulation of CD8+ T cell function, complete transcriptomes of eIF3d-inhibited Jurkat T cells were sequenced by RNA sequencing (RNA-Seq). Additionally, to examine the effect of eIF3d on CD8+ T cell function, eIF3d expression was inhibited alone or in combination with SOCS-7 knockdown by siRNA in isolated CD8+ T cells. CD8+ T cell proliferation, IFN-r secretion and apoptosis were detected by flow cytometry. Moreover, the effect of eIF3d on HIV replication was evaluated in Jurkat cells, peripheral blood mononuclear cells (PBMCs) and CD4+ T cells with eIF3d knockdown using a pNL4-3 pseudotyped virus. Results At approximately 100 days of infection, only eIF3d was markedly decreased in RPs compared with chronic progressors (CPs). Expression of eIF3d correlated significantly with disease progression in EHI. Based on in vitro analyses, reduced eIF3d expression led to decreased proliferation and IFN-γ secretion and increased apoptosis in CD8+ T cells. Inhibited expression of eIF3d caused enhanced expression of SOCS-7, and inhibiting SOCS-7 expression by siRNA rescued the attenuated CD8+ T cell function caused by eIF3d. Finally, when eIF3d was inhibited in Jurkat cells, PBMCs and CD4+ T cells, pNL4-3-VSV-G virus replication was enhanced. Conclusions The current data highlight the importance of eIF3d in HIV infection by inhibiting CD8+ T cell function and promoting viral replication. Our study provides potential targets for improved immune intervention. Electronic supplementary material The online version of this article (10.1186/s12967-019-1925-0) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 66%

Reduced eIF3d accelerates HIV disease progression by attenuating CD8+ T cell function

et al. 2019

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“…The overexpression of eIF3D has been observed to promote cell proliferation, migration, or/and tumour growth in several cancer entities, including ovarian cancer [31], renal cell carcinoma [32], gastric cancer (GC) [33], and gallbladder cancer (GBC) [34]. As being discovered in our study, all these high levels of eIF3D are associated with advanced tumour stage, indicating its potential role in tumour development.…”

Section: Discussionsupporting

confidence: 70%

Overexpression of eIF3D in Lung Adenocarcinoma Is a New Independent Prognostic Marker of Poor Survival

et al. 2019

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The eukaryotic initiation factor 3 (eIF3) is the largest and most complex translation initiation factor in mammalian cells. It consists of 13 subunits and among which several were implicated to have significant prognostic effects on multiple human cancer entities. To examine the expression profiles of eIF3 subunits and determine their prognostic value in patients with lung adenocarcinoma (LUAD), the genomic data, survival data, and related clinical information were obtained from The Cancer Genome Atlas (TCGA) project for a secondary analysis. The results showed that among ten aberrantly expressed eIF3 subunits in tumours compared with adjacent normal counterparts (p < 0.05), only upregulated eIF3D could predict poor overall survival (OS) outcome independent of multiple clinicopathological parameters (HR = 2.043, 95% CI: 1.132-3.689, p = 0.018). Chi-square analysis revealed that the highly expressed eIF3D group had larger ratios of patients with advanced pathological stage (68/40 vs. 184/206, p = 0.0046), residual tumour (13/4 vs. 163/176, p = 0.0257), and targeted molecular therapy (85/65 vs. 138/164, p = 0.0357). In silico analysis demonstrated that the altered expression of eIF3D was at least regulated by both copy number alterations (CNAs) and the hypomethylation of cg14297023 site. In conclusion, high eIF3D expression might serve as a valuable independent prognostic indicator of shorter OS in patients with LUAD.

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“…The majority of GC patients are diagnosed at an advanced stage and receive a poor prognosis (20). One of the reasons for the poor outcomes of GC is the malignant biological behaviors of GC cells, particularly for those with low-to-intermediate differentiation stages, which often possess strong abilities in proliferation, migration, invasion and tumorigenesis (21,22).…”

Section: Discussionmentioning

confidence: 99%

NFIB promotes cell growth, aggressiveness, metastasis and EMT of gastric cancer through the Akt/Stat3 signaling pathway

Zhu

Liu

et al. 2018

Oncol Rep

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Nuclear factor I/B (NFIB) plays a crucial role in the progression of several types of cancers. However, its role in gastric cancer (GC) remains unclear. The present study revealed that NFIB was highly expressed in GC tissues and was positively associated with the clinicopathological features of GC patients. Downregulation of NFIB inhibited the tumor growth, migration and aggression of MKN45 and HGC27 cells in vitro. In addition, NFIB expression promoted epithelial‑mesenchymal transition (EMT), which was accompanied with decreased E‑cadherin and increased vimentin expression. Since AKT and Stat3 play an important role in EMT and tumor progression, we examined whether there is a correlation between NFIB and AKT/Stat3 signaling pathways in GC. Our results revealed that NFIB exhibits its oncogenic functions in GC development by regulating the phosphorylation of both AKT and Stat3 molecules. Knocking down the NFIB expression may enhance the phosphorylation of AKT while inhibiting the Stat3 phosphorylation, suggesting that the AKT/Stat3 signaling pathway may be the downstream target of NFIB with which it exerts its roles on GC development. These results revealed that NFIB promotes tumor growth and aggressiveness of GC. In addition, downregulation of NFIB alters the protein kinase B/signal transducers and activators of transcription 3 (AKT/Stat3) axis, which could be a potential molecular mechanism for precise target treatment of GC.

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High expression of eIF3d is associated with poor prognosis in patients with gastric cancer

Cited by 18 publications

References 24 publications

Reduced eIF3d accelerates HIV disease progression by attenuating CD8+ T cell function

Reduced eIF3d accelerates HIV disease progression by attenuating CD8+ T cell function

Overexpression of eIF3D in Lung Adenocarcinoma Is a New Independent Prognostic Marker of Poor Survival

NFIB promotes cell growth, aggressiveness, metastasis and EMT of gastric cancer through the Akt/Stat3 signaling pathway

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