Evidence map›Paper›PMID 26393798›Full record

ArticlePloS one2015

c-Myc Represses Tumor-Suppressive microRNAs, let-7a, miR-16 and miR-29b, and Induces Cyclin D2-Mediated Cell Proliferation in Ewing's Sarcoma Cell Line.

Masanori Kawano, Kazuhiro Tanaka, Ichiro Itonaga, Tatsuya Iwasaki, Hiroshi Tsumura

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. 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
1.9field-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, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Epigenetic Control of Translation Checkpoint and Tumor Progression via RUVBL1-EEF1A1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  10. Article
  11. Review
  12. Systems Biology Analysis for Ewing Sarcoma.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  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. Article
  20. Non-Coding RNAs in Pediatric Solid Tumors.Frontiers in genetics · 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

5 authors at 1 institution in 1 country.

Masanori KawanoDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, Japan.
Kazuhiro TanakaDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, Japan.
Ichiro ItonagaDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, Japan.
Tatsuya IwasakiDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, Japan.
Hiroshi TsumuraDepartment of Orthopaedic Surgery, Faculty of Medicine, Oita University, Oita, Japan.
Oita University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myc oncogenic transcription factor is known to inhibit tumor suppressive microRNAs (miRNAs), resulting in greater expression of their target protein related to cell cycle, invasion or anti-apoptotic factors in human cancer cells. To explore possible oncogenic factors in Ewing's sarcoma (ES), we conducted microarray-based approach to profile the changes in the expression of miRNAs and its downstream mRNAs in five ES cell lines and human mesenchymal stem cells (hMSCs). Three miRNAs, let-7a, miR-16 and miR-29b were significantly down-regulated, whereas c-Myc and cyclin D2 (CCND2) were significantly up-regulated in all tested ES cells compared with hMSCs. To verify that let-7a, miR-16 and miR-29b were the targets of c-Myc in ES cell lines, we transfected siRNA against c-Myc and confirmed the coordinate up-regulation of let-7a, miR-16 and miR-29b through the repression of c-Myc. The ES cells transfected with c-Myc-siRNA and let-7a, miR-16 and miR-29b exhibited the inhibition of the cell cycle progression. The increased expression of let-7a, miR-16 and miR-29b resulted in the reduction of CCND2 protein expression. We also demonstrated that c-Myc-siRNA treatment of ES cells was associated with the decreased expression of CCND2 as a down-stream of three miRNAs. Furthermore, the introduction of let-7a, miR-16 and miR-29b in ES cells could inhibit the c-Myc-mediated up-regulation of CCND2 resulted in the prevention of cell cycle progression. In addition, the transfection of let-7a, miR-16 and miR-29b in ES cells suppressed tumor growth ex vivo treatment. These findings suggests that the up-regulation of c-Myc inhibited the expression of let-7a, miR-16 and miR-29b subsequently induced CCND2 expression in ES cells. The present study might identify a novel oncogenic axis that c-Myc regulates the expression of CCND2 via let-7a, miR-16 and miR-29b, leading to the development new therapeutic targets for ES.

Indexed as

AnimalsCell CycleCell Line, TumorCell ProliferationCyclin D2Down-RegulationGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansMesenchymal Stem CellsMiceMice, Inbred BALB CMice, NudeMicroRNAsProto-Oncogene Proteins c-mycRNA, MessengerCyclin D2MicroRNAsProto-Oncogene Proteins c-mycRNA, MessengerRNA, Small Interfering

Identifiers

PMID26393798
PMCPMC4578885
OpenAlexW2188203081

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.