Evidence map›Paper›PMID 34016142›Full record

ArticleJournal of translational medicine2021

eIF6 promotes the malignant progression of human hepatocellular carcinoma via the mTOR signaling pathway.

Liping Sun, Shuguang Liu, Xiaopai Wang, Xuefeng Zheng, Ya Chen, Hong Shen

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 5 institutions in 1 country.

Liping Sun *Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Shuguang LiuDepartment of Pathology, The Eighth Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.
Xiaopai WangDepartment of Pathology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, China.
Xuefeng ZhengDepartment of Anatomy, Neuroscience Laboratory for Cognitive and Developmental Disorders, Medical College of Jinan University, Guangzhou, China.
Ya ChenDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Hong ShenDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. shenhong2010168@163.com.ORCID 0000-0001-5345-4709
Southern Medical University · CNGuangzhou First People's Hospital · CNJinan University · CNNanfang Hospital · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEukaryotic translation initiation factor 6 (eIF6) has a crucial function in the maturation of 60S ribosomal subunits, and it controls the initiation of protein translation. Although emerging studies indicate that eIF6 is aberrantly expressed in various types of cancers, the functions and underlying molecular mechanisms of eIF6 in the pathological progression of hepatocellular carcinoma (HCC) remain unclear. This study aimed to evaluate the potential diagnostic and prognostic value of eIF6 in patients with HCC.

methodsHCC samples enrolled from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO) and our cohort were used to explore the role and mechanism of eIF6 in HCC. The diagnostic power of eIF6 was verified by receiver operating characteristic curve (ROC) analysis and its prognostic value was assessed by Kaplan-Meier analysis, and then related biological functions of eIF6 were determined in vitro and in vivo cancer models. In addition, potential molecular mechanism of eIF6 in HCC was unveiled by the gene set enrichment analysis and western blot assay.

resultsWe demonstrated that eIF6 expression was markedly increased in HCC, and elevated eIF6 expression correlated with pathological progression of HCC. Besides, eIF6 served as not only a new diagnostic biomarker but also an independent risk factor for OS in HCC patients. Functional studies indicated that the deletion of eIF6 displayed tumor-suppressor activity in HCC cells. Furthermore, we found that eIF6 could activate the mTOR-related signaling pathway and regulate the expression level of its target genes, such as CCND1, CDK4, CDK6, MYC, CASP3 and CTNNBL1, and these activities promoted proliferation and invasion of HCC cells.

conclusionsThe findings of this study provided a novel basis for understanding the potential role of eIF6 in promoting tumor growth and invasion, and exploited a promising strategy for improving diagnosis and prognosis of HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsEukaryotic Initiation FactorsGene Expression Regulation, NeoplasticHumansPrognosisSignal TransductionTOR Serine-Threonine KinasesEIF6 protein, humanEukaryotic Initiation FactorsMTOR protein, humanTOR Serine-Threonine KinasesCell proliferationEIF6Hepatocellular carcinomaMTORPrognosis

Identifiers

PMID34016142
PMCPMC8139032
OpenAlexW3161100926

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.