Evidence map›Paper›PMID 17906696›Full record

ArticleOncogene2008

c-Myc depletion inhibits proliferation of human tumor cells at various stages of the cell cycle.

H Wang, S Mannava, V Grachtchouk, D Zhuang, M S Soengas, A V Gudkov, E V Prochownik, M A Nikiforov

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

112 citing papers in PubMed, 172 citations in OpenAlex.

  1. Article
  2. Article
  3. Dual-action peptide KWHVeterinary research · 2026
    Article
  4. c-Myc: an emerging participant in heart failure.Frontiers in cardiovascular medicine · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Manipulating Myc for reparative regeneration.Frontiers in cell and developmental biology · 2024
    Review
  17. Article
  18. Article
  19. Article
  20. Article

52 more citing papers are in PubMed but not listed here.

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 4 institutions in 1 country.

H WangSection of Hematology/Oncology, Children's Hospital of Pittsburgh, Rangos Research Center, Pittsburgh, PA, USA.
S Mannava
V Grachtchouk
D Zhuang
M S Soengas
A V Gudkov
E V Prochownik
M A Nikiforov
University of Michigan–Ann Arbor · USBoston Children's Hospital · USChildren's Hospital of Pittsburgh · USCleveland Clinic Lerner College of Medicine · US

Funding

Oncogene c-Myc-dependent pathways in cutaneous melanoma03R01CA120244 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NIKIFOROV, MIKHAIL · 2007 to 2016
$3.3M
Structure-based design of novel low molecular weight c-Myc inhibitorsR01CA140624 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PROCHOWNIK, EDWARD VICTOR · 2009 to 2013
$2.7M
C-, N-, AND L-MYC EFFECTS ON HEMATOPOIETIC CELLSR01CA078259 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PROCHOWNIK, EDWARD VICTOR · 1999 to 2009
$2.0M
Regulation of and by the Myc OncoproteinR01CA105033 · NCI · CHILDREN'S HOSP PITTSBURGH/UPMC HLTH SYS · PI PROCHOWNIK, EDWARD VICTOR · 2004 to 2008
$1.4M
Apoptosis in Melanoma Progression and ChemoresistanceR01CA107237 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SOENGAS, MARIA S · 2004 to 2008
$1.3M
NCI NIH HHS R01 CA078259NCI NIH HHS R01-CA078259NCI NIH HHS R01 CA105033NCI NIH HHS R01-CA105033NCI NIH HHS R01 CA107237NCI NIH HHS R01 CA120244NCI NIH HHS R01-CA120244-A1NCI NIH HHS R01 CA140624
6 · The paper itself

Abstract

A major role for c-Myc in the proliferation of normal cells is attributed to its ability to promote progression through G(1) and into S phase of the cell cycle. The absolute requirement of c-Myc for cell cycle progression in human tumor cells has not been comprehensively addressed. In the present work, we used a lentiviral-based short hairpin RNA (shRNA) expression vector to stably reduce c-Myc expression in a large number of human tumor cell lines and in three different types of normal human cells. In all cases, cell proliferation was severely inhibited, with normal cells ultimately undergoing G(0)/G(1) growth arrest. In contrast, tumor cells demonstrated a much more variable cell cycle response with cells from several lines accumulating in S or G(2)/M phases. Moreover, in some tumor lines, the phase of cell cycle arrest caused by inhibition of c-Myc could be altered by depleting tumor suppressor protein p53 or its transcriptional target p21(CIP/WAF). Our data suggest that, as in the case of normal cells, c-Myc is essential for sustaining proliferation of human tumor cells. However its rate-limiting role in cell cycle control is variable and is reliant upon the status of other cell cycle regulators.

Indexed as

Cell ProliferationCell CycleCells, CulturedCyclin-Dependent Kinase Inhibitor p21FibroblastsFlow CytometryGreen Fluorescent ProteinsHumansImmunoblottingKeratinocytesMelanocytesNeoplasmsProto-Oncogene Proteins c-mycRNA, Small InterferingTumor Suppressor Protein p53CDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21enhanced green fluorescent proteinGreen Fluorescent ProteinsMYC protein, humanProto-Oncogene Proteins c-mycRNA, Small InterferingTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID17906696
PMCPMC3144565
OpenAlexW2080903787

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.