Evidence map›Paper›PMID 27122673›Full record

ArticleWorld journal of gastroenterology2016

Eukaryotic elongation factor-1α 2 knockdown inhibits hepatocarcinogenesis by suppressing PI3K/Akt/NF-κB signaling.

Fu-Nan Qiu, Yi Huang, Dun-Yan Chen, Feng Li, Yan-An Wu, Wen-Bing Wu, Xiao-Li Huang

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  3. EEF1A2 identified as a hub gene associated with the severity of metabolic dysfunction-associated steatotic liver disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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  8. Review
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  11. eEF1A2 siRNA Suppresses MPPTheScientificWorldJournal · 2023
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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

7 authors at 2 institutions in 1 country.

Fu-Nan QiuFu-Nan Qiu, Yi Huang, Dun-Yan Chen, Feng Li, Yan-An Wu, Wen-Bing Wu, Xiao-Li Huang, Provincial Clinical College, Fujian Medical University, Fuzhou 350001, Fujian Province, China.
Yi HuangFu-Nan Qiu, Yi Huang, Dun-Yan Chen, Feng Li, Yan-An Wu, Wen-Bing Wu, Xiao-Li Huang, Provincial Clinical College, Fujian Medical University, Fuzhou 350001, Fujian Province, China.
Dun-Yan ChenFu-Nan Qiu, Yi Huang, Dun-Yan Chen, Feng Li, Yan-An Wu, Wen-Bing Wu, Xiao-Li Huang, Provincial Clinical College, Fujian Medical University, Fuzhou 350001, Fujian Province, China.
Feng LiFu-Nan Qiu, Yi Huang, Dun-Yan Chen, Feng Li, Yan-An Wu, Wen-Bing Wu, Xiao-Li Huang, Provincial Clinical College, Fujian Medical University, Fuzhou 350001, Fujian Province, China.
Yan-An WuFu-Nan Qiu, Yi Huang, Dun-Yan Chen, Feng Li, Yan-An Wu, Wen-Bing Wu, Xiao-Li Huang, Provincial Clinical College, Fujian Medical University, Fuzhou 350001, Fujian Province, China.
Wen-Bing WuFu-Nan Qiu, Yi Huang, Dun-Yan Chen, Feng Li, Yan-An Wu, Wen-Bing Wu, Xiao-Li Huang, Provincial Clinical College, Fujian Medical University, Fuzhou 350001, Fujian Province, China.
Xiao-Li HuangFu-Nan Qiu, Yi Huang, Dun-Yan Chen, Feng Li, Yan-An Wu, Wen-Bing Wu, Xiao-Li Huang, Provincial Clinical College, Fujian Medical University, Fuzhou 350001, Fujian Province, China.
Fujian Provincial Hospital · CNFujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo assess the impact of eukaryotic elongation factor 1 alpha 2 (eEF1A2) on hepatocellular carcinoma (HCC) cell proliferation, apoptosis, migration and invasion, and determine the underlying mechanisms.

methodseEF1A2 levels were detected in 62 HCC tissue samples and paired pericarcinomatous specimens, and the human HCC cell lines SK-HEP-1, HepG2 and BEF-7402, by real-time PCR and immunohistochemistry. Experimental groups included eEF1A2 silencing in BEL-7402 cells with lentivirus eEF1A2-shRNA (KD group) and eEF1A2 overexpression in SK-HEP-1 cells with eEF1A2 plasmid (OE group). Non-transfected cells (control group) and lentivirus-based empty vector transfected cells (NC group) were considered control groups. Cell proliferation (MTT and colony formation assays), apoptosis (Annexin V-APC assay), cell cycle (DNA ploidy assay), and migration and invasion (Transwell assays) were assessed. Protein levels of PI3K/Akt/NF-κB signaling effectors were evaluated by Western blot.

resultseEF1A2 mRNA and protein levels were significantly higher in HCC cancer tissue samples than in paired pericarcinomatous and normal specimens. SK-HEP-1 cells showed lower eEF1A2 mRNA levels; HepG2 and BEL-7402 cells showed higher eEF1A2 mRNA levels, with BEL-7402 cells displaying the highest amount. Efficient eEF1A2 silencing resulted in reduced cell proliferation, migration and invasion, increased apoptosis, and induced cell cycle arrest. The PI3K/Akt/NF-κB signaling pathway was notably inhibited. Inversely, eEF1A2 overexpression resulted in promoted cell proliferation, migration and invasion.

conclusioneEF1A2, highly expressed in HCC, is a potential oncogene. Its silencing significantly decreases HCC tumorigenesis, likely by inhibiting PI3K/Akt/NF-κB signaling.

Indexed as

AdolescentAdultAgedApoptosisCarcinoma, HepatocellularCase-Control StudiesCell Cycle CheckpointsCell MovementCell ProliferationDown-RegulationFemaleGene Expression Regulation, NeoplasticHep G2 CellsHumansLiver NeoplasmsMaleEEF1A2 protein, humanNF-kappa BPeptide Elongation Factor 1Phosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktRNA, MessengerCarcinogenesisEukaryotic elongation factor 1 alpha 2Hepatocellular carcinomaPI3K/Akt/NF-κB signaling pathwayProliferation

Identifiers

PMID27122673
PMCPMC4837440
OpenAlexW2342583611

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.