Evidence map›Paper›PMID 23468863›Full record

ArticlePloS one2013

Akt2 regulates metastatic potential in neuroblastoma.

Jingbo Qiao, Sora Lee, Pritha Paul, Lan Qiao, Chase J Taylor, Cameron Schlegel, Nadja C Colon, Dai H Chung

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Peptidergic Systems and Neuroblastoma.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Diverse roles of miR-335 in development and progression of cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  16. Article
  17. miR-302b suppresses cell invasion and metastasis by directly targeting AKT2 in human hepatocellular carcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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

8 authors at 1 institution in 1 country.

Jingbo QiaoDepartment of Pediatric Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Sora Lee
Pritha Paul
Lan Qiao
Chase J Taylor
Cameron Schlegel
Nadja C Colon
Dai H Chung
Vanderbilt University Medical Center · US

Funding

Surgical Oncology Training GrantT32CA106183 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI James Richard Goldenring · 2004 to 2026
$6.0M
Surgical Studies on the Role on Gastrin-releasing Peptide in NeuroblastomaR01DK061470 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI CHUNG, DAI H. · 2003 to 2018
$4.7M
NCI NIH HHS T32 CA106183NIDDK NIH HHS R01 DK061470NIDDK NIH HHS R01 DK61470
6 · The paper itself

Abstract

Activation of PI3K/AKT pathway correlates with poor prognosis in patients with neuroblastoma. Our previous studies have demonstrated that PI3K/AKT signaling is critical for the oncogenic transformations induced by gastrin-releasing peptide (GRP) and its receptor, GRP-R, in neuroblastoma. Moreover, PI3K/AKT-dependent oncogenic transformations require N-myc, an extensively studied oncogene in neuroblastoma. Whether AKT directly regulates the expression of N-myc oncogene is yet to be determined. Here, we report a novel finding that of the three AKT isoforms, AKT2 specifically regulated N-myc expression in neuroblastoma cells. We also confirmed that GRP-R is upstream of AKT2 and in turn, regulated N-myc expression via AKT2 in neuroblastoma cells. Functional assays demonstrated that attenuation of AKT2 impaired cell proliferation and anchorage-independent cell growth, and decreased the secretion of angiogenic factor VEGF in vitro. Furthermore, silencing AKT2 inhibited migration and invasion of neuroblastoma cells in vitro. Xenografts established by injecting AKT2 silenced human neuroblastoma cells into murine spleen expressed decreased levels of AKT2 and resulted in fewer liver metastases compared to controls in vivo. Hence, our study highlights the potential molecular mechanism(s) mediating the oncogenic role of GRP/GRP-R and demonstrates a novel role for AKT2 in neuroblastoma tumorigenesis, indicating that targeting the GRP/GRP-R/AKT2 axis may be important for developing novel therapeutics in the treatment of clinically aggressive neuroblastoma.

Indexed as

AnimalsCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalGene Expression Regulation, NeoplasticGene SilencingGenes, mycHumansLiver NeoplasmsMaleMiceNeoplasm MetastasisNeuroblastomaProto-Oncogene Proteins c-aktReceptors, G-Protein-CoupledAKT2 protein, humanProto-Oncogene Proteins c-aktReceptors, G-Protein-Coupled

Identifiers

PMID23468863
PMCPMC3582607
OpenAlexW2025844474

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.