Evidence map›Paper›PMID 10557096›Full record

ArticleOncogene1999

Induction of tumor suppression and glandular differentiation of A549 lung carcinoma cells by dominant-negative IGF-I receptor.

Y Jiang, W N Rom, T A Yie, C X Chi, K M Tchou-Wong

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. The impact of the IGF-1 system of cancer cells on radiation response - AnClinical and translational radiation oncology · 2017
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
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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

5 authors at 2 institutions in 1 country.

Y JiangDepartment of Medicine, Division of Pulmonary and Critical Care Medicine, New York University Medical Center, 550 First Avenue, MSB 147, New York, NY 10016, USA.
W N Rom
T A Yie
C X Chi
K M Tchou-Wong
New York University · USColumbia University Irving Medical Center · US

Funding

ZOPOLRESTAT IN SUBJECTS W/ PERIPHERAL SYMMETRICAL DIABETIC POLYNEUROPATHYM01RR000096 · NCRR · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NOVIK, YELENA · 1985 to 2008
$34.8M
HOST RESPONSE TO TB AND AIDSR01HL059832 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ROM, WILLIAM N · 1997 to 2006
$3.6M
IMMUNE RESPONSE IN THE LUNG TO TB PROTEINS IN AIDSR01HL062055 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ROM, WILLIAM N · 1998 to 2002
$990k
NCRR NIH HHS MO1-RR00096NHLBI NIH HHS R01-HL59832NHLBI NIH HHS R01-HL62055
6 · The paper itself

Abstract

Overexpression or activation of insulin-like growth factor I receptor (IGF-IR) has been observed in many human cancers including breast, lung, colon and gastric carcinomas. We demonstrate that inhibition of the endogenous insulin-like growth factor I receptor by stable expression of a dominant-negative IGF-IR represses the transforming activity in vitro and tumorigenicity of human lung carcinoma cells A549 in vivo. The suppression of tumorigenicity in nude mice is correlated with the induction of glandular differentiation. In addition, functional inhibition of the endogenous receptor dramatically increases the sensitivity of A549 cells to a variety of apoptotic signals including UV irradiation and proteasome inhibitors. These effects are due to the formation of a stable heterocomplex of the dominant-negative receptor with the endogenous wild type receptor which reduces the kinase activity of the latter by twofold. Thus, inhibition of the IGF-IR signaling pathway not only suppresses tumorigenicity but also enhances sensitivity to apoptosis-inducing agents. Antagonizing IGF-IR signaling by promoting tumor differentiation and enhancing sensitivity to apoptotic death are potential cancer therapeutic approaches.

Indexed as

Genes, Tumor SuppressorAcetylcysteineAdenocarcinomaAnimalsApoptosisCarcinogenicity TestsCell DifferentiationCell DivisionCysteine EndopeptidasesCysteine Proteinase InhibitorsGenes, DominantHumansLeupeptinsLung NeoplasmsMiceMice, NudeAcetylcysteinebenzyloxycarbonylleucyl-leucyl-leucine aldehydeCysteine EndopeptidasesCysteine Proteinase InhibitorslactacystinLeupeptinsMultienzyme ComplexesProteasome Endopeptidase ComplexReceptor, IGF Type 1

Identifiers

PMID10557096
OpenAlexW1981661908

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.