Evidence map›Paper›PMID 31235829›Full record

ArticleScientific reports2019

miRNA-302s may act as oncogenes in human testicular germ cell tumours.

Mrinal K Das, Herman S F Evensen, Kari Furu, Trine B Haugen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Role of SPRY4 in health and disease.Frontiers in oncology · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. miRNA in Molecular Diagnostics.Bioengineering (Basel, Switzerland) · 2022
    Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

4 authors at 1 institution in 1 country.

Mrinal K DasFaculty of Health Sciences, OsloMet - Oslo Metropolitan University, Oslo, Norway. m.k.das@medisin.uio.no.
Herman S F EvensenFaculty of Health Sciences, OsloMet - Oslo Metropolitan University, Oslo, Norway.
Kari FuruFaculty of Health Sciences, OsloMet - Oslo Metropolitan University, Oslo, Norway.
Trine B HaugenFaculty of Health Sciences, OsloMet - Oslo Metropolitan University, Oslo, Norway.
OsloMet – Oslo Metropolitan University · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Testicular germ cell tumour (TGCT) represents the most common malignancy in young men in large parts of the world, but the aetiology is yet unclear. Multiple TGCT susceptibility loci have been identified, and we have shown that one of these, SPRY4, may act as a TGCT oncogene. Furthermore, many of the loci are in non-coding regions of the genome. miRNAs, a class of non-coding RNAs may play a crucial role in cell proliferation, differentiation, and apoptosis, and alteration in their expression may lead to oncogenesis. Differential expression of miRNAs in TGCT and normal testis has been reported in previous studies. In this study, we used qPCR to analyse, in normal and malignant testis tissue, the expression of the ten miRNAs that we had previously identified by sequencing to be the most upregulated in TGCT. We found high expression of these miRNAs also by qPCR analysis. The levels of miR-302a-3p, miR-302b-3p, and miR-302c-3p were downregulated after treatment of the TGCT cell lines NT2-D1 and 833 K with the chemotherapy drug cisplatin. By using miRNA inhibitor-mediated transient transfection, we inhibited the expression of the three members of miR-302 family (miR-302s). Inhibition of miR-302s resulted in a decreased cell proliferation in NT2-D1 cells, but not in 833 K cells. In both cell lines, inhibition of miR-302s resulted in decreased expression of SPRY4, which we have previously shown to regulate MAPK/ERK and PI3K/Akt signalling pathways in these cells. Inhibition of miR-302b-3p and miR-302c-3p decreased phosphorylation of ERK1/2, whereas inhibition of miR-302a-3p and miR-302b-3p led to decreased expression of the apoptosis inhibitor, survivin. Our findings suggest that miR-302s act as TGCT oncogenes by inducing the expression of SPRY4 and activating MAPK/ERK pathway while inhibiting apoptosis via increased survivin expression.

Indexed as

CarcinogenesisAntineoplastic AgentsCarcinoma, EmbryonalCell Line, TumorCell ProliferationCisplatinDrug Resistance, NeoplasmHumansMaleMicroRNAsNeoplasms, Germ Cell and EmbryonalSeminomaTesticular NeoplasmsAntineoplastic AgentsCisplatinMicroRNAsMIRN302A microRNA, human

Identifiers

PMID31235829
PMCPMC6591358
OpenAlexW2950053207

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.