Evidence map›Paper›PMID 34150009›Full record

ArticleAmerican journal of translational research2021

Highly enriched exosomal lncRNA OIP5-AS1 regulates osteosarcoma tumor angiogenesis and autophagy through miR-153 and ATG5.

Yumei Li, Shengming Lin, Xiaoliang Xie, Haixia Zhu, Tianyou Fan, Song Wang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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  8. Exosomal Gene Biomarkers in Osteosarcoma: Mifepristone as a Targeted Therapeutic Revealed by Multi-Omics Analysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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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

6 authors at 1 institution in 1 country.

Yumei LiDepartment of Orthopedics, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine 274 Zhijiang Central Road, Jingan District, Shanghai 200071, China.
Shengming LinDepartment of Radiology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine 725 Wanping South Road, Xuhui District, Shanghai 200032, China.
Xiaoliang XieDepartment of Orthopedics, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine 274 Zhijiang Central Road, Jingan District, Shanghai 200071, China.
Haixia ZhuDepartment of Orthopedics, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine 274 Zhijiang Central Road, Jingan District, Shanghai 200071, China.
Tianyou FanDepartment of Orthopedics, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine 274 Zhijiang Central Road, Jingan District, Shanghai 200071, China.
Song WangDepartment of Radiology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine 725 Wanping South Road, Xuhui District, Shanghai 200032, China.
Shanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study aims to investigate the regulatory role of exosome lncRNA OIP5-AS1 in tumor progression and autophagy.

methodsSeventy-three cases of osteosarcoma (OS) tissues and 56 cases of adjacent normal tissues were collected to culture human OS cell line HOS. The exosomes secreted by OS cell line were isolated and collected. Apoptosis and exosome markers were detected by flow cytometry. A nude mouse model of OS was established. The gene expression levels of lncRNA OIP5-AS1, miR-153 and autophagy-related protein 5 (ATG5) were quantified by real-time quantitative PCR (RT-PCR). The binding sites of lncRNA OIP5-AS1 and miR-153 were predicted by Starbase3.0, and the binding sites of miR-153 and ATG5 were predicted by Targetscan7.2. The gene binding sites were verified by luciferase reporter gene detection or RNA immunoprecipitation (RIP). The relative level of protein was tested by Western blot. Transwell was applied to test migration and invasion of OS cells. The angiogenesis of OS cells was tested by tubule formation test.

resultsThe results of RT-PCR showed that lncRNA OIP5-AS1 levels were elevated in OS cells and exosomes secreted by cells. Cell function experiments revealed that the proliferation, migration, and invasion of OS cells were promoted by exosomal lncRNA OIP5-AS1. In exosomes, lncRNA OIP5-AS1 inhibited the expression of LC3-II and Beclin 1 proteins, indicating that exosomal lncRNA OIP5-AS1 inhibited autophagy. According to the results of bioinformatics tools and dual-luciferase reporter (DLR) assay or RNA immunoprecipitation (RIP), miR-153 targeted the 3'-UTR of lncRNA OIP5-AS1 and autophagy-related protein 5 (ATG5). The results of western blot (WB) assay showed that exosomal lncRNA OIP5-AS1 and down-regulated miR-153 led to the enhancement of ATG5 protein expression, while up-regulated miR-153 resulted in the decrease of ATG5 protein expression. ATG5 was negatively correlated with miR-153 and positively correlated with lncRNA OIP5-AS1. The results of tubule formation assay disclosed an increase in the angiogenesis level caused by the exosomal lncRNA OIP5-AS1, which was then reversed by the increase of miR-153 and decrease of ATG5.

conclusionHighly enriched exosomal lncRNA OIP5-AS1 can regulate OS tumor angiogenesis and autophagy through miR-153 and ATG5.

Indexed as

angiogenesisATG5autophagyexosomal lncRNA OIP5miR-153Osteosarcoma

Identifiers

PMID34150009
PMCPMC8205742
OpenAlexW3174482926

What OpenQuestion holds

Textmetadata
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.