Evidence map›Paper›PMID 28138700›Full record

ArticleMolecular medicine reports2017

MicroRNA-410 regulates autophagy-related gene ATG16L1 expression and enhances chemosensitivity via autophagy inhibition in osteosarcoma.

Ren Chen, Xiaohai Li, Bin He, Wei Hu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  10. Virus, Exosome, and MicroRNA: New Insights into Autophagy.Advances in experimental medicine and biology · 2022
    Article
  11. Review
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  17. miRNA signatures in childhood sarcomas and their clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019
    Review
  18. Review
  19. Review
  20. Role of autophagy in osteosarcoma.Journal of bone oncology · 2019
    Review
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 2 institutions in 1 country.

Ren ChenDepartment of Spine Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Xiaohai LiDepartment of Spine Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Bin HeDepartment of Spine Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Wei HuDepartment of Spine Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Wuhan University · CNRenmin Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma, which is the most common type of primary bone tumor in adolescents, is characterized by complex genetic alterations and frequent resistance to conventional treatments. MicroRNAs (miRs) have emerged as fundamental regulators in gene expression through their ability to silence gene expression at post-transcriptional and translational levels. The present study investigated the role of miR‑410 in the progression of osteosarcoma. The results demonstrated that the expression of miR‑410 was markedly downregulated in human osteosarcoma tissues, and U2OS and MG‑63 osteosarcoma cell lines. Clinicopathological significance suggested that miR‑410 may be a potential biomarker for chemotherapy‑resistant osteosarcoma. Furthermore, overexpression of miR‑410 exhibited a limited effect on cell viability in U2OS and MG‑63 cells. Target prediction algorithms (TargetScan and miRanda) indicated that autophagy related 16‑like 1 (ATG16L1) was a potential target gene of miR‑410. A luciferase reporter assay demonstrated that miR‑410 directly decreased ATG16L1 expression by targeting its 3'‑untranslated region. In addition, the results revealed that miR‑410 was able to markedly inhibit autophagy. Accordingly, autophagy was activated as a protective mechanism when osteosarcoma cells were exposed to three common anticancer drugs, including rapamycin, doxorubicin and cisplatin. Furthermore, the autophagy inhibitor 3‑methyladenine and miR‑410 expression were able to improve the therapeutic response of the cells to chemotherapy drugs (rapamycin, doxorubicin and cisplatin), thus indicating that miR‑410 enhanced chemosensitivity through autophagy inhibition in osteosarcoma cells. In conclusion, studies regarding the function of miR‑410 on autophagy provided insight into the biological function of miR‑410 in osteosarcoma and may offer a promising approach for the treatment of osteosarcoma.

Indexed as

AdenineAdultAntineoplastic AgentsAutophagyAutophagy-Related ProteinsBiomarkersBone NeoplasmsCell Line, TumorDoxorubicinDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansMaleMicroRNAsNeoplasm Staging3-methyladenineAdenineAntineoplastic AgentsATG16L1 protein, humanAutophagy-Related ProteinsBiomarkersDoxorubicinMicroRNAsMIRN410 microRNA, human

Identifiers

PMID28138700
PMCPMC5367354
OpenAlexW2581999303

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.