Evidence map›Paper›PMID 18283312›Full record

ArticleBritish journal of cancer2008

Growth inhibition of non-small cell lung cancer cells by AP-1 blockade using a cJun dominant-negative mutant.

Y Shimizu, I Kinoshita, J Kikuchi, K Yamazaki, M Nishimura, M J Birrer, H Dosaka-Akita

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Claudins 10 and 18 are predominantly expressed in lung adenocarcinomas and in tumors of nonsmokers.International journal of clinical and experimental pathology · 2011
    Article
  9. A dominant-negative c-jun mutant inhibits lung carcinogenesis in mice.Cancer prevention research (Philadelphia, Pa.) · 2010
    Article
  10. Article
  11. Review
  12. Article
  13. 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 3 institutions in 2 countries.

Y ShimizuDepartment of Medical Oncology, Hokkaido University Graduate School of Medicine, North 15, West 7, Kita-ku, Sapporo 060-8638, Japan.
I Kinoshita
J Kikuchi
K Yamazaki
M Nishimura
M J Birrer
H Dosaka-Akita
Hokkaido University · JPSapporo Medical University · JPCenter for Cancer Research · US

Funding

USE OF TRANSCRIPTIONAL FACTORS AS TARGETS AND AGENTS IN CARCINOGENESISZ01SC000165 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI BIRRER, MICHAEL · 1996 to 2008
$974k
The Use of Transcriptional Factors as Targets and Agents in CarcinogenesisZIASC000165 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI BIRRER, MICHAEL · 2009 to 2009
$187k
6 · The paper itself

Abstract

cJun, a major constituent of AP-1 transcription factor transducing multiple mitogen growth signals, is frequently overexpressed in non-small cell lung cancers (NSCLCs). The purpose of this study is to determine the effects of AP-1 blockade on the growth of NSCLC cells using a cJun dominant-negative mutant, TAM67. Transiently transfected TAM67 inhibited AP-1 transcriptional activity in NSCLC cell lines, NCI-H1299 (H1299), A549 and NCI-H520 (H520). The colony-forming efficiency of H1299 and A549 was reduced by TAM67, while that of H520 was not. To elucidate the effects of TAM67 on the growth of H1299, we established H1299 clone cells that expressed TAM67 under the control of a doxycycline-inducible promoter. In the H1299 clone cells, the induced TAM67 inhibited anchorage-dependent growth by promoting G1 cell-cycle block, but not by apoptosis. The induced TAM67 decreased the expression of a cell-cycle regulatory protein, cyclin A. TAM67 also inhibited anchorage-independent growth of these cells. Furthermore, TAM67 reduced growth of established xenograft tumours from these cells in nude mice. These results suggest that AP-1 plays an essential role in the growth of at least some of NSCLC cells.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungDNAFemaleG1 PhaseGenetic TherapyHumansLung NeoplasmsMiceMice, Inbred BALB CNeoplasm TransplantationPeptide FragmentsProto-Oncogene Proteins c-junTranscription Factor AP-1Transplantation, HeterologousDNAPeptide FragmentsProto-Oncogene Proteins c-junTAM67 peptideTranscription Factor AP-1

Identifiers

PMID18283312
PMCPMC2266861
OpenAlexW1965904488

What OpenQuestion holds

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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.