Evidence map›Paper›PMID 19540207›Full record

ArticleBiochemical pharmacology2009

N-Myc down regulation induced differentiation, early cell cycle exit, and apoptosis in human malignant neuroblastoma cells having wild type or mutant p53.

Rajiv Janardhanan, Naren L Banik, Swapan K Ray

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Biochemical pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Modulation of Notch Signaling Pathway by Bioactive Dietary Agents.International journal of molecular sciences · 2022
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  9. Role of retinoids in the prevention and treatment of colorectal cancer.World journal of gastrointestinal oncology · 2015
    Review
  10. MYCN concurrence with SAHA-induced cell death in human neuroblastoma cells.Cellular oncology (Dordrecht, Netherlands) · 2015
    Article
  11. Using CellMiner 1.6 for Systems Pharmacology and Genomic Analysis of the NCI-60.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015
    Review
  12. Article
  13. Article
  14. Article
  15. Article
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  17. Article
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Rajiv JanardhananDepartment of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, 6439 Garners Ferry Road, Columbia, SC 29209, USA.
Naren L Banik
Swapan K Ray
University of South Carolina · USMedical University of South Carolina · US

Funding

DIFFERENTIATION AND APOPTOSIS IN MALIGNANT NEUROBLASTOMAR01NS057811 · NINDS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI RAY, SWAPAN K. · 2006 to 2009
$1.3M
PROTEOLYTIC CONTROL OF GLIOBLASTOMAR01CA091460 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI RAY, SWAPAN K · 2003 to 2007
$1.1M
NCI NIH HHS CA-91460NCI NIH HHS R01 CA091460NINDS NIH HHS NS-57811NINDS NIH HHS R01 NS057811
6 · The paper itself

Abstract

Neuroblastomas, which mostly occur in children, are aggressive metastatic tumors of the sympathetic nervous system. The failure of the previous therapeutic regimens to target multiple components of N-Myc pathway resulted in poor prognosis. The present study investigated the efficacy of the combination of N-(4-hydroxyphenyl) retinamide (4-HPR, 0.5 microM) and genistein (GST, 25 microM) to control the growth of human neuroblastoma cells (SH-SY5Y and SK-N-BE2) harboring divergent molecular attributes. Combination of 4-HPR and GST down regulated N-Myc, Notch-1, and Id2 to induce neuronal differentiation. Transition to neuronal phenotype was accompanied by increase in expression of e-cadherin. Induction of neuronal differentiation was associated with decreased expression of hTERT, PCNA, survivin, and fibronectin. This is the first report that combination of 4-HPR and GST mediated reactivation of multiple tumor suppressors (p53, p21, Rb, and PTEN) for early cell cycle exit (due to G1/S phase arrest) in neuroblastoma cells. Reactivation of tumor suppressor(s) repressed N-Myc driven growth factor mediated angiogenic and invasive pathways (VEGF, b-FGF, MMP-2, and MMP-9) in neuroblastoma. Repression of angiogenic factors led to the blockade of components of mitogenic pathways [phospho-Akt (Thr 308), p65 NF-kappaB, and p42/44 Erk 1/2]. Taken together, the combination of 4-HPR and GST effectively blocked survival, mitogenic, and angiogenic pathways and activated proteases for apoptosis in neuroblastoma cells. These results suggested that combination of 4-HPR and GST could be effective for controlling the growth of heterogeneous human neuroblastoma cell populations.

Indexed as

Genes, p53MutationApoptosisCell CycleCell DifferentiationCell Line, TumorFenretinideFlow CytometryGlutathione TransferaseHumansNeuroblastomaProto-Oncogene Proteins c-mycSignal TransductionFenretinideGlutathione TransferaseProto-Oncogene Proteins c-myc

Identifiers

PMID19540207
PMCPMC3103941
OpenAlexW2156055427

What OpenQuestion holds

Textmetadata
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.