Evidence map›Paper›PMID 27120793›Full record

ArticleOncotarget2016

Downregulation of miRNA-638 promotes angiogenesis and growth of hepatocellular carcinoma by targeting VEGF.

Jiwen Cheng, Yanke Chen, Pu Zhao, Xi Liu, Jian Dong, Jianhui Li, Chen Huang, Rongqian Wu, Yi Lv

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. miRNAs in HCC, pathogenesis, and targets.Hepatology (Baltimore, Md.) · 2024
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  3. Review
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  13. Noncoding RNAs: the shot callers in tumor immune escape.Signal transduction and targeted therapy · 2020
    Review
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  15. Article
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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

9 authors at 4 institutions in 1 country.

Jiwen ChengDepartment of Hepatobiliary Surgery, Institute of Advanced Surgical Technology and Engineering, First Affiliated Hospital of Xi'an Jiaotong University, Xi' an, Shaanxi, China.
Yanke ChenDepartment of Genetics and Cell Biology, Environment and Genes Related to Diseases Key Laboratory of Education Ministry, College of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Pu ZhaoDepartment of Neonatology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China.
Xi LiuDepartment of Pathology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Jian DongDepartment of Hepatobiliary Surgery, Institute of Advanced Surgical Technology and Engineering, First Affiliated Hospital of Xi'an Jiaotong University, Xi' an, Shaanxi, China.
Jianhui LiDepartment of Surgical Oncology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China.
Chen HuangDepartment of Genetics and Cell Biology, Environment and Genes Related to Diseases Key Laboratory of Education Ministry, College of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Rongqian WuDepartment of Hepatobiliary Surgery, Institute of Advanced Surgical Technology and Engineering, First Affiliated Hospital of Xi'an Jiaotong University, Xi' an, Shaanxi, China.
Yi LvDepartment of Hepatobiliary Surgery, Institute of Advanced Surgical Technology and Engineering, First Affiliated Hospital of Xi'an Jiaotong University, Xi' an, Shaanxi, China.
First Affiliated Hospital of Xi'an Jiaotong University · CNXi'an Jiaotong University · CNShaanxi Provincial People's Hospital · CNShanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression and function of microRNA-638 (miR-638) in hepatocellular carcinoma (HCC) remained unknown. Using the miRNA target prediction tools, we predicted that the vascular endothelial growth factor (VEGF) might be a direct target of miR-638. The aim of this study was to test the hypothesis that downregulation of miRNA-638 promotes angiogenesis and growth of HCC by targeting the VEGF signaling pathway. We found that miR-638 was significantly downregulated in HCC cells and clinical HCC specimens, and miR-638 levels were inversely correlated with tumor size, portal vein invasion and poor prognosis. Overexpression of miR-638 inhibited the processes of tumor angiogenesis in vitro and in vivo. The xenograft mouse model experiments showed miR-638 repressed tumor growth of HCC in vivo. Using a luciferase reporter assay, we identified VEGF as a direct target of miR-638. Subsequent investigation revealed that miR-638 expression was inversely correlated with VEGF expression in human HCC samples. Taken together, these results suggested that miR-638 is a novel therapeutic target for HCC and overexpression of miR-638 could suppress angiogenesis and tumor growth of HCC by inhibiting VEGF signaling.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinogenesisCarcinoma, HepatocellularDown-RegulationFemaleHep G2 CellsHumansLiver NeoplasmsMaleMiceMice, Inbred BALB CMice, NudeMicroRNAsMiddle AgedNeovascularization, PathologicMicroRNAsMIRN638 microRNA, humanVascular Endothelial Growth Factor AVEGFA protein, humanangiogenesishepatocellular carcinomamiR-638prognosisvascular endothelial growth factor

Identifiers

PMID27120793
PMCPMC5058711
OpenAlexW2341459510

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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.