Evidence map›Paper›PMID 32022476›Full record

ArticleCancer medicine2020

Long noncoding RNA DUXAP8 contributes to the progression of hepatocellular carcinoma via regulating miR-422a/PDK2 axis.

Feifei Wei, Liang Yang, Dandan Jiang, Min Pan, Guiyan Tang, Mingyue Huang, Jing Zhang

Abstract read
In one paragraph

Article in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

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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

23 citing papers in PubMed.

  1. Functional, Pharmacogenomic, and Immune Landscapes of Long Non-Coding RNAs in Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  9. LncRNAFrontiers in genetics · 2022
    Article
  10. LncRNA-DUXAP8 Regulation of the Wnt/β-Catenin Signaling Pathway to Inhibit Glycolysis and Induced Apoptosis in Acute Myeloid LeukemiaTurkish journal of haematology : official journal of Turkish Society of Haematology · 2021
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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.

Feifei WeiDepartment of Oncology, Fifth Clinical Medical College, Guilin Medical University, Guilin, People's Republic of China.
Liang YangDepartment of Oncology, Fifth Clinical Medical College, Guilin Medical University, Guilin, People's Republic of China.
Dandan JiangDepartment of Oncology, Jining NO.1 People's Hospital; Affiliated Jining NO.1 People's Hospital, Jining Medical University, Jining, People's Republic of China.ORCID 0000-0003-0517-3042
Min PanDepartment of Oncology, Fifth Clinical Medical College, Guilin Medical University, Guilin, People's Republic of China.
Guiyan TangDepartment of Oncology, Fifth Clinical Medical College, Guilin Medical University, Guilin, People's Republic of China.
Mingyue HuangDepartment of Oncology, Fifth Clinical Medical College, Guilin Medical University, Guilin, People's Republic of China.
Jing ZhangDepartment of Oncology, Fifth Clinical Medical College, Guilin Medical University, Guilin, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is one of the most deadly cancer worldwide. Multiple long noncoding RNAs (lncRNAs) are recently identified as crucial oncogenic factors or tumor suppressors. In this study, we explored the functon and mechanism of lncRNA double homeobox A pseudogene 8 (DUXAP8) in the progression of HCC.

methodsExpression levels of DUXAP8 in HCC tissue samples were measured using qRT-PCR. The association between pathological indexes and the expression of DUXAP8 was also analyzed. Human HCC cell lines SMMC-7721 and QSG-7701 were used in in vitro studies. CCK-8 assay was used to assess the effect of DUXAP8 on HCC cell line proliferation. Scratch healing assay and Transwell assay were conducted to detect the effect of DUXAP8 on migration and invasion. Furthermore, dual-luciferase reporter assay was used to confirm targeting relationship between miR-422a and DUXAP8. Additionally, Western blot was used to detect the regulatory function of DUXAP8 on pyruvate dehydrogenase kinase 2 (PDK2).

resultsDUXAP8 expression HCC clinical samples was significantly increased and this was correlated with unfavorable pathological indexes. High expression of DUXAP8 was associated with shorter overall survival time of patients. Its overexpression remarkably facilitated the proliferation, metastasis, and epithelial-mesenchymal transition of HCC cells. Accordingly, knockdown of it suppressed the malignant phenotypes of HCC cells. Overexpression of DUXAP8 significantly reduced the expression of miR-422a by sponging it, but enhanced the expression of PDK2.

conclusionsDUXAP8 was a sponge of tumor suppressor miR-422a in HCC, enhanced the expression of PDK2 indirectly, and functioned as an oncogenic lncRNA.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisBiomarkers, TumorCarcinoma, HepatocellularCell ProliferationFemaleHumansLiver NeoplasmsMaleMicroRNAsMiddle AgedPrognosisPyruvate Dehydrogenase Acetyl-Transferring KinaseRNA, Long NoncodingSurvival RateTumor Cells, CulturedBiomarkers, TumorMicroRNAsMIRN422 microRNA, humanPDK2 protein, humanPyruvate Dehydrogenase Acetyl-Transferring KinaseRNA, Long NoncodingDUXAP8HCCmiR-422aPDK2

Identifiers

PMID32022476
PMCPMC7131864

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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.