Evidence map›Paper›PMID 32968448›Full record

ArticleOncology letters2020

MicroRNA-615 functions as a tumor suppressor in osteosarcoma through the suppression of HK2.

Limin Sun, Peng Wang, Zhiqiang Zhang, Kai Zhang, Zheng Xu, Siyuan Li, Junsheng Mao

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Metabolic reprogramming in osteosarcoma.Pediatric discovery · 2023
    Review
  6. Decoding the regulatory roles of non-coding RNAs in cellular metabolism and disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. The roles of glycolysis in osteosarcoma.Frontiers in pharmacology · 2022
    Review
  15. Review
  16. Article
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

7 authors at 2 institutions in 1 country.

Limin SunDepartment of Orthopedics, Shandong Provincial Third Hospital, Jinan, Shandong 250031, P.R. China.
Peng WangDepartment of Orthopedics, Shandong Provincial Third Hospital, Jinan, Shandong 250031, P.R. China.
Zhiqiang ZhangDepartment of Orthopedics, Shandong Provincial Third Hospital, Jinan, Shandong 250031, P.R. China.
Kai ZhangDepartment of Orthopedics, Shandong Provincial Third Hospital, Jinan, Shandong 250031, P.R. China.
Zheng XuDepartment of Orthopedics, Shandong Provincial Third Hospital, Jinan, Shandong 250031, P.R. China.
Siyuan LiDepartment of Orthopedics, Shandong Provincial Third Hospital, Jinan, Shandong 250031, P.R. China.
Junsheng MaoDepartment of Orthopedic Surgery, Taishan Hospital of Shandong Province, Tai'an, Shandong 271000, P.R. China.
Shandong Provincial Hospital · CNAffiliated Hospital of Taishan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At present, the regulatory mechanisms of various microRNAs (miRNAs/miRs) have been elucidated in human cancers including osteosarcoma (OS). This study mainly focused on the role of miR-615 in OS, which has not yet been reported. Ninety-two OS tissues and normal samples were used in this study. Human osteoblast hFOB1.19 cells and OS cell line HOS were utilized to detect the expression of miR-615. The expression of miR-615 and gene expression were assessed by RT-qPCR and western blot analysis. Transwell, MTT and luciferase reporter assays were used to investigate the regulatory mechanism of miR-615 in OS. The results revealed that miR-615 expression was reduced in OS tissues and cells, and was associated with poor clinical outcomes and prognosis in OS patients. In addition, overexpression of miR-615 restrained cell viability and metastasis in OS. Furthermore, hexokinase 2 (HK2) was confirmed as a direct target of miR-615. Upregulation of HK2 was detected in OS tissues. The upregulation of HK2 weakened the tumor-suppressive effect of miR-615 in OS. Moreover, miR-615 blocked epithelial-mesenchymal transition (EMT) and inactivated the PI3K/AKT pathway in OS. To conclude, miR-615 acts as a tumor suppressor in OS, thus miR-615 can be used as a target for OS treatment.

Indexed as

HK2metastasismiR-615osteosarcomaPI3K/AKT pathwayproliferation

Identifiers

PMID32968448
PMCPMC7500052
OpenAlexW3085228594

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.