Evidence map›Paper›PMID 30038373›Full record

ArticleScientific reports2018

Biostatistics mining associated method identifies AKR1B10 enhancing hepatocellular carcinoma cell growth and degenerated by miR-383-5p.

Junqing Wang, Yunyun Zhou, Xiaochun Fei, Xuehua Chen, Yongjun Chen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  10. Aldo-keto Reductase 1B10 Restrains Cell Migration, Invasion, and Adhesion of Gastric Cancer via Regulating Integrin Subunit Alpha 5.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
    Article
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  16. MicroRNA-383: A tumor suppressor miRNA in human cancer.Frontiers in cell and developmental biology · 2022
    Review
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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

5 authors at 2 institutions in 2 countries.

Junqing WangDepartment of Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197, Rui Jin Er Road, Shanghai, 20025, People's Republic of China. wangjunqingmd@hotmail.com.ORCID 0000-0001-6874-9614
Yunyun ZhouDepartment of Data Science, University of Mississippi Medical Center, Jackson, MS, 39216, USA.
Xiaochun FeiDepartment of Pathology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197, Rui Jin Er Road, Shanghai, 20025, People's Republic of China.
Xuehua ChenShanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197, Rui Jin Er Road, Shanghai, 20025, People's Republic of China.
Yongjun ChenDepartment of Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197, Rui Jin Er Road, Shanghai, 20025, People's Republic of China. cyj10651@rjh.com.cn.
Shanghai Jiao Tong University · CNJackson Memorial Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have reported that the aberrantly expressed AKR1B10 is associated with many cancer development, however the functional roles of AKR1B10 and its regulatory mechanisms in hepatocellular carcinoma (HCC) have been limited studied. In this project, we identified AKR1B10 functional as an oncogene in HCC through tumor/normal human tissue comparison from both GEO microarray and TCGA RNAseq dataset. Further experimental validations from three HCC cell lines (SMMC-7721, HePG2 and HeP3B) also suggested the ontogenetic functions of AKR1B10 in HCC tumor growth. By knocking down AKR1B10 through shRNA in HCC HeP3B cells, we showed it significantly induced cell cycle arrest and inhibited cell growth. Interestingly, integrative analysis of TCGA RNAseq data and miRNA-seq data predicted that miR-383-5p, a novel post-transcriptional tumor suppressor, is negatively associated with AKR1B10 expression. To further investigate the role of miR-383-5p in regulating AKR1B10 in HCC, we performed Dual-luciferase reporter assay experiments. Results showed that miR-383-5p is an upstream modulator targeting AKR1B10 in the post-transcriptional stage. Thus, we report AKR1B10 modulated regulated by miR-383-5p, promotes HCC tumor progress, and could be potentially a therapeutic target for precision medicine in HCC.

Indexed as

BiostatisticsData MiningAldehyde ReductaseAldo-Keto ReductasesCarcinoma, HepatocellularCell Cycle CheckpointsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansLiver NeoplasmsMicroRNAsProtein Interaction MappingRNA, MessengerTranscription, GeneticAKR1B10 protein, humanAldehyde ReductaseAldo-Keto ReductasesMicroRNAsMIRN383 microRNA, humanRNA, Messenger

Identifiers

PMID30038373
PMCPMC6056456
OpenAlexW2884353092

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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.