Evidence map›Paper›PMID 16359544›Full record

ArticleBMC cancer2005

Introduction of in vitro transcribed ENO1 mRNA into neuroblastoma cells induces cell death.

Katarina Ejeskär, Cecilia Krona, Helena Carén, Faten Zaibak, Lingli Li, Tommy Martinsson, Panayiotis A Ioannou

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. ENO1 and Cancer.Molecular therapy oncolytics · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Serodiagnostic Potential of Alpha-Enolase FromFrontiers in microbiology · 2018
    Article
  19. [Role of enolase 1 in hepatocellular carcinoma and possible mechanism].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2017
    Article
  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

7 authors at 4 institutions in 2 countries.

Katarina EjeskärDept, Clinical Genetics, University of Gothenburg, Sahlgrenska University Hospital/East, SE-416 85 Gothenburg, Sweden. katarina.ejeskar@clingen.gu.se
Cecilia Krona
Helena Carén
Faten Zaibak
Lingli Li
Tommy Martinsson
Panayiotis A Ioannou
Royal Children's Hospital · AUSahlgrenska University Hospital · SEUniversity of Gothenburg · SEUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuroblastoma is a solid tumour of childhood often with an unfavourable outcome. One common genetic feature in aggressive tumours is 1p-deletion. The alpha-enolase (ENO1) gene is located in chromosome region 1p36.2, within the common region of deletion in neuroblastoma. One alternative translated product of the ENO1 gene, known as MBP-1, acts as a negative regulator of the c-myc oncogene, making the ENO1 gene a candidate as a tumour suppressor gene.

methodsMethods used in this study are transfection of cDNA-vectors and in vitro transcribed mRNA, cell growth assay, TUNEL-assay, real-time RT-PCR (TaqMan) for expression studies, genomic sequencing and DHPLC for mutation detection.

resultsHere we demonstrate that transfection of ENO1 cDNA into 1p-deleted neuroblastoma cell lines causes' reduced number of viable cells over time compared to a negative control and that it induces apoptosis. Interestingly, a similar but much stronger dose-dependent reduction of cell growth was observed by transfection of in vitro transcribed ENO1 mRNA into neuroblastoma cells. These effects could also be shown in non-neuroblastoma cells (293-cells), indicating ENO1 to have general tumour suppressor activity. Expression of ENO1 is detectable in primary neuroblastomas of all different stages and no difference in the level of expression can be detected between 1p-deleted and 1p-intact tumour samples. Although small numbers (11 primary neuroblastomas), there is some evidence that Stage 4 tumours has a lower level of ENO1-mRNA than Stage 2 tumours (p = 0.01). However, mutation screening of 44 primary neuroblastomas of all different stages, failed to detect any mutations.

conclusionOur studies indicate that ENO1 has tumour suppressor activity and that high level of ENO1 expression has growth inhibitory effects.

Indexed as

ApoptosisTranscription, GeneticApoptosis Regulatory ProteinsBiomarkers, TumorCell LineCell Line, TumorCell ProliferationDNA-Binding ProteinsDNA, ComplementaryDNA Mutational AnalysisGene DeletionGenes, Tumor SuppressorGenetic VectorsGenomeHumansIn Situ Nick-End LabelingApoptosis Regulatory ProteinsBiomarkers, TumorDNA-Binding ProteinsDNA, ComplementaryENO1 protein, humanPhosphopyruvate HydrataseRNA, MessengerRNA, Small InterferingTumor Suppressor Proteins

Identifiers

PMID16359544
PMCPMC1327688
OpenAlexW1545790360

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.