Evidence map›Paper›PMID 33121268›Full record

ArticleCell transplantation

LncRNA GAS5 Suppresses the Proliferation and Invasion of Osteosarcoma Cells via the miR-23a-3p/PTEN/PI3K/AKT Pathway.

Jianmin Liu, Ming Chen, Longyang Ma, Xingbo Dang, Gongliang Du

Open access · goldAbstract read
In one paragraph

Article in Cell transplantation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  6. Epigenetic Regulation by lncRNA GAS5/miRNA/mRNA Network in Human Diseases.International journal of molecular sciences · 2025
    Review
  7. Review
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  9. Article
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  11. LncRNACentral-European journal of immunology · 2024
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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 1 institution in 1 country.

Jianmin LiuDepartment of Emergency Surgery, Shaanxi Provincial People's Hospital (Affiliated Hospital of Xi'an Medical University), Xi'an, China.
Ming ChenDepartment of Orthopedics, Shaanxi Provincial People's Hospital (Affiliated Hospital of Xi'an Medical University), Xi'an, China.ORCID 0000-0002-2487-3514
Longyang MaDepartment of Emergency Surgery, Shaanxi Provincial People's Hospital (Affiliated Hospital of Xi'an Medical University), Xi'an, China.
Xingbo DangDepartment of Emergency Surgery, Shaanxi Provincial People's Hospital (Affiliated Hospital of Xi'an Medical University), Xi'an, China.
Gongliang DuDepartment of Emergency Surgery, Shaanxi Provincial People's Hospital (Affiliated Hospital of Xi'an Medical University), Xi'an, China.
Shaanxi Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence has shown that long noncoding RNA GAS5 is a well-known tumor suppressor in the pathogenesis of a variety of human cancers. However, the detailed role of GAS5 in osteosarcoma is still largely unclear. In this study, we found that GAS5 was downregulated in human osteosarcoma tissues and cell lines compared with matched adjacent tissues and normal osteoblast cells. Overexpression of GAS5 could significantly suppress the growth and invasion of osteosarcoma cells, while downregulation of GAS5 promoted cell proliferation and invasion. We confirmed that GAS5 could directly bind with miR-23a-3p by using luciferase reporter gene and RNA immunoprecipitation and pull-down assay. Downregulation of miR-23a-3p repressed cell proliferation and invasion. Overexpression of miR-23a-3p counterbalanced the inhibition effect of GAS5 on cell proliferation and invasion. Further studies indicated that overexpression of GAS5 inhibited cell proliferation and metastasis by regulating phosphatase and tensin homolog (PTEN). PTEN was authenticated as a target of miR-23a-3p. Upregulation of GAS5 or silence of miR-23a-3p increased the level of PTEN, while downregulation of GAS5 or overexpression of miR-23a-3p suppressed the expression of PTEN. In addition, overexpression of GAS5 could neutralize the effect of downregulating PTEN on osteosarcoma cell functions. We proved that GAS5 regulated the viability and invasion of osteosarcoma cells through the PI3K/AKT pathway. Moreover, overexpression of GAS5 could inhibit tumor growth in a xenograft nude mouse model in vivo. In summary, GAS5 functions as a competing endogenous RNA, sponging miR-23a-3p, to promote PTEN expression and suppress cell growth and invasion in osteosarcoma by regulating the PI3K/AKT pathway.

Indexed as

AnimalsBase SequenceCarcinogenesisCell Line, TumorCell MovementCell ProliferationDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansMaleMice, Inbred BALB CMice, NudeMicroRNAsNeoplasm InvasivenessOsteosarcomaGAS5 long non-coding RNA, humanMicroRNAsMIRN23a microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanRNA, Long Noncodinggrowth arrest special 5long noncoding RNAmiR-23a-3posteosarcomaphosphatase and tensin homolog

Identifiers

PMID33121268
PMCPMC7784500
OpenAlexW3095452002

What OpenQuestion holds

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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.