Evidence map›Paper›PMID 29410498›Full record

ArticleScientific reports2018

Knockdown of SPRY4 and SPRY4-IT1 inhibits cell growth and phosphorylation of Akt in human testicular germ cell tumours.

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

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 19% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Overlapping genetic etiology of pediatric and adult germ cell tumors.Journal of the National Cancer Institute · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Role of SPRY4 in health and disease.Frontiers in oncology · 2024
    Review
  11. Article
  12. Article
  13. Epigenetic Factors and ncRNAs in Testicular Cancer.International journal of molecular sciences · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Bioengineered · 2022
    Article
  19. Review
  20. 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 2 countries.

Mrinal K DasFaculty of Health Sciences, OsloMet - Oslo Metropolitan University, Oslo, Norway. mrinal-kumar.das@hioa.no.ORCID http://orcid.org/0000-0002-7749-7591
Kari FuruFaculty of Health Sciences, OsloMet - Oslo Metropolitan University, Oslo, Norway.
Herman F EvensenFaculty of Health Sciences, OsloMet - Oslo Metropolitan University, Oslo, Norway.
Øyvind P HaugenFaculty 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) is the most common cancer in young men in large parts of the world, but the aetiology is mainly unknown. Genome-wide association studies have so far identified about 50 susceptibility loci associated with TGCT, including SPRY4. SPRY4 has shown tumour suppressor activity in several cancer cells, such as lung and prostate, while it was found to act as an oncogene in ovarian cancer. An intronic region within the SPRY4 gene produces a long non-coding RNA, SPRY4-IT1, which has been reported to act as an oncogene in melanoma, breast cancer, and colorectal cancer, and as a tumour suppressor in lung cancer. The roles of SPRY4 and SPRY4-IT1 in TGCT development are yet unknown. We found higher expression levels of SPRY4, both mRNA and protein, and of SPRY4-IT1 in human TGCT than in normal adult testis. Small-interfering RNA (siRNA)-mediated transient knockdown of SPRY4 and SPRY4-IT1 in two TGCT cell lines 833 K and NT2-D1 resulted in decreased cell growth, migration, and invasion. Knockdown of SPRY4 and SPRY4-IT1 also led to a significant reduction in the phosphorylation of Akt. Our findings indicate that SPRY4 and SPRY4-IT1 may act as oncogenes in TGCTs via activation of the PI3K / Akt signalling pathway.

Indexed as

Gene Expression Regulation, NeoplasticGenome, HumanAdultCase-Control StudiesCell Line, TumorCell ProliferationGenetic LociHumansIntracellular Signaling Peptides and ProteinsMaleNeoplasms, Germ Cell and EmbryonalNerve Tissue ProteinsOrgan TransplantationPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktIntracellular Signaling Peptides and Proteinslong noncoding RNA SPRY4-IT1, humanNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingRNA, Small InterferingSPRY4 protein, human

Identifiers

PMID29410498
PMCPMC5802735
OpenAlexW2805818946

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.