Evidence map›Paper›PMID 31564967›Full record

ArticleCancer management and research2019

Long noncoding RNA MIR31HG abrogates the availability of tumor suppressor microRNA-361 for the growth of osteosarcoma.

Yongjie Sun, Xinghao Jia, Mingxing Wang, Yiqi Deng

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer management and research, 2019. 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
1.8field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  10. Host gene and its guest: short story about relation of long-noncodingReports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2023
    Review
  11. Article
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  13. Long Non-Coding RNAInternational journal of molecular sciences · 2022
    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

4 authors at 1 institution in 1 country.

Yongjie SunDepartment of Orthopedics, Shanxian Central Hospital Affiliated to Jining Medical University, Heze, Shandong 274300, People's Republic of China.
Xinghao JiaDepartment of Orthopedics, Shanxian Haijiya Hospital, Heze, Shandong 274300, People's Republic of China.
Mingxing WangDepartment of Orthopedics, Shanxian Central Hospital Affiliated to Jining Medical University, Heze, Shandong 274300, People's Republic of China.
Yiqi DengDepartment of Orthopedics, Shanxian Central Hospital Affiliated to Jining Medical University, Heze, Shandong 274300, People's Republic of China.ORCID 0000-0003-3492-5303
Xian Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeLong noncoding RNA (LncRNA) containing microRNA host gene is an interesting type of LncRNA. MicroRNA-31 (miR-31)-host gene LncRNA (MIR31HG) have been recognized as an oncogene in many cancers, but not in osteosarcoma (OS). Interestingly, MIR31HG/miR-31 could not regulate each other's expression in certain cancer, suggesting that the role of MIR31HG in cancer is independent of miR-31. We here investigated the function and potential mechanism of MIR31HG in OS.

methodsOS tissues and adjacent non-tumor tissues (n=40) were collected to determine the expressions of MIR31HG by paired

resultsMIR31HG was upregulated in OS tissues and OS cell lines. The patients with high expression of MIR31HG have high tumor stages and distant metastasis. Tumor suppressor miR-361, but not miR-31, was confirmed to be sponged directly by MIR31HG in OS cells and was down-regulated in OS cell lines. Knockdown of MIR31HG restored the expression of miR-361. Restoration of miR-361 level in Saos-2 and U2OS cells induced cell apoptosis and G1/S arrest, inhibited proliferation and migration, which was, however, abrogated by MIR31HG. Mechanistically, cell growth and metastasis-related target genes of MIR-361 including VEGF, FOXM1 and Twist were de-repressed in OS cells by MIR31HG overexpression, leading to upregulated BCL2, CCND1 and epithelial-mesenchymal transition (EMT) phenotype. Patients with high expression of MIR31HG also showed more VEGF, FOXM1 and Twist levels. Overexpression of MIR31HG in vivo also promoted tumor growth via inhibition of miR-361 signals and elevated the expression of VEGF, FOXM1 and Twist for tumor growth.

conclusionMIR31HG acts as an oncogene in OS for tumor progression via regulation of tumor suppressor miR-361 and its target genes.

Indexed as

LncRNAsMIR31HGmiR-361osteosarcomaproliferation

Identifiers

PMID31564967
PMCPMC6722458
OpenAlexW2971257303

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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.