Evidence map›Paper›PMID 32412676›Full record

ArticleMolecular oncology2020

Long non-coding RNA PGM5-AS1 promotes epithelial-mesenchymal transition, invasion and metastasis of osteosarcoma cells by impairing miR-140-5p-mediated FBN1 inhibition.

Wei Liu, Pengcheng Liu, Hang Gao, Xu Wang, Ming Yan

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Molecular oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
2.2field-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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  7. Review
  8. The extracellular matrix glycoprotein fibrillin-1 in health and disease.Frontiers in cell and developmental biology · 2023
    Review
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  10. Article
  11. The FAPActa pharmaceutica Sinica. B · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Wei LiuDepartment of Spine Surgery, The First Hospital of Jilin University, Changchun, China.
Pengcheng LiuDepartment of Hand and Foot Surgery, The First Hospital of Jilin University, Changchun, China.
Hang GaoDepartment of Bone and Joint Surgery, The First Hospital of Jilin University, Changchun, China.
Xu WangDepartment of Colorectal and Anal Surgery, The First Hospital of Jilin University, Changchun, China.
Ming YanDepartment of Spine Surgery, The First Hospital of Jilin University, Changchun, China.ORCID 0000-0002-9762-4471
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma is an uncommon tumor occurring in bone, accompanied by elevated incidence and reduced rate of healing. Epithelial-to-mesenchymal transition (EMT) serves as a conceptual paradigm to explain the invasion and metastasis of osteosarcoma and other cancers. Hence, developing effective therapeutic strategy to treat the EMT of osteosarcoma is essential. Here, we identified the molecular mechanism of long noncoding RNA (lncRNA) PGM5-AS1 in EMT and progression of osteosarcoma. Microarray-based analysis was employed to screen the osteosarcoma-related differentially expressed lncRNAs. The levels of PGM5-AS1 as well as microRNA-140-5p (miR-140-5p) and fibrillin-1 (FBN1) in osteosarcoma tissues and cells were determined. Dual-luciferase reporter gene assay, RNA pull-down assay, and RNA immunoprecipitation assay were conducted to validate the relationship among PGM5-AS1, miR-140-5p, and FBN1. Expression of PGM5-AS1, miR-140-5p, and FBN1 was altered by overexpression, shRNA, mimic, or inhibitors in order to investigate how they regulated migration, invasion, and EMT of osteosarcoma cells in vitro. Loss- and gain-of-function approaches were employed in nude mice to detect their roles in tumorigenesis in vivo. Osteosarcoma tissues and cells exhibited low expression of miR-140-5p, but high expression of PGM5-AS1 and FBN1. PGM5-AS1 competitively bound to miR-140-5p to upregulate FBN1. Furthermore, hindering PGM5-AS1 and FBN1 or overexpressing miR-140-5p dampened migration, invasion, and EMT of osteosarcoma cells in vitro. Furthermore, silencing PGM5-AS1 or FBN1, or overexpressing miR-140-5p markedly inhibited tumorigenesis in nude mice in vivo. Taken together, PGM5-AS1 depletion causes FBN1 reduction to retard osteosarcoma processes by negatively modulating miR-140-5p.

Indexed as

AdipokinesAnimalsBase SequenceCarcinogenesisCell Line, TumorCell MovementDisease ProgressionEpithelial-Mesenchymal TransitionFemaleFibrillin-1Gene Expression Regulation, NeoplasticGene SilencingHumansMaleMice, NudeMicroRNAsAdipokinesFBN1 protein, humanFibrillin-1MicroRNAsMirn140 microRNA, humanRNA, Long Noncodingfibrillin-1long noncoding RNA PGM5-AS1microRNA-140-5posteosarcoma

Identifiers

PMID32412676
PMCPMC7530781
OpenAlexW3024977989

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.