Evidence map›Paper›PMID 18281471›Full record

ArticleCancer research2008

Growth suppression of lung cancer cells by targeting cyclic AMP response element-binding protein.

Sita Aggarwal, Seung-Wook Kim, Seung-Hee Ryu, Wen-Cheng Chung, Ja Seok Koo

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

56 citing papers in PubMed, 89 citations in OpenAlex.

  1. cAMP response element-binding protein promotes gliomagenesis by modulating the expression of oncogenic microRNA-23a.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Trial
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  6. Aging, adaptation and maladaptation.Frontiers in aging · 2023
    Article
  7. Article
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  9. SS18-SSX drives CREB activation in synovial sarcoma.Cellular oncology (Dordrecht, Netherlands) · 2022
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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 1 institution in 1 country.

Sita AggarwalDepartment of Thoracic/Head and Neck Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
Seung-Wook Kim
Seung-Hee Ryu
Wen-Cheng Chung
Ja Seok Koo
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Targeting the p53 pathway for reversal of oral premalignancyP50CA097007 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MYERS, JEFFREY NICHOLAS · 2002 to 2012
$26.1M
Role of CREB in Lung Cancer DevelopmentR01CA126801 · NCI · YALE UNIVERSITY · PI KOO, JA SEOK · 2010 to 2014
$1.6M
CREB in Differentiation of Bronchial Mucous CellsR01HL077556 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KOO, JA SEOK · 2004 to 2007
$1.3M
NCI NIH HHS CA-16672NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA097007NCI NIH HHS R01 CA126801NHLBI NIH HHS R01 HL077556NHLBI NIH HHS R01-HL-077556
6 · The paper itself

Abstract

Genes regulated by cyclic AMP-response element-binding protein (CREB) have been reported to suppress apoptosis, induce cell proliferation, and mediate inflammation and tumor metastasis. However, it is not clear whether CREB is critically involved in lung carcinogenesis. We found that non-small cell lung cancer (NSCLC) cell lines exhibited elevated constitutive activity in CREB, in its immediate upstream kinases (ribosomal s6 kinase and extracellular signal kinase), and in the CREB-regulated cell survival proteins Bcl-2 and Bcl-xL. We hypothesized that constitutively active CREB is important to lung cancer cell growth and survival and therefore could be a potential therapeutic target for NSCLC. Ectopic expression of dominant repressor CREB and transfection with small interfering RNA against CREB suppressed the growth and survival of NSCLC cells and induced apoptotic cell death. Furthermore, treating H1734 NSCLC cells with an inhibitor of the CREB signaling pathway Ro-31-8220 inhibited CREB activation by blocking the activity of extracellular signal kinase and ribosomal s6 kinase, arrested the cell cycle at the G(2)-M phase, and subsequently induced apoptosis with the suppression of Bcl-2 and Bcl-xL expression. Ro-31-8220 suppressed both the anchorage-dependent and independent growth of NSCLC cells, but its cytotoxic effect was much less prominent in normal bronchial epithelial cells. Our results indicate that active CREB plays an important role in NSCLC cell growth and survival. Thus, agents that suppress CREB activation could have potential therapeutic value for NSCLC treatment.

Indexed as

ApoptosisCarcinoma, Non-Small-Cell LungCell DivisionCell Growth ProcessesCell Line, TumorCyclic AMP Response Element-Binding ProteinG2 PhaseHumansIndolesLung NeoplasmsPhosphorylationSignal TransductionCyclic AMP Response Element-Binding ProteinIndolesRo 31-8220

Identifiers

PMID18281471
PMCPMC2921320
OpenAlexW2133088932

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.