Evidence map›Paper›PMID 21525012›Full record

ArticleThe Journal of biological chemistry2011

Epidermal growth factor receptor-mediated tissue transglutaminase overexpression couples acquired tumor necrosis factor-related apoptosis-inducing ligand resistance and migration through c-FLIP and MMP-9 proteins in lung cancer cells.

Zi Li, Xiuling Xu, Lang Bai, Wenshu Chen, Yong Lin

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
8.5field-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

47 citing papers in PubMed, 74 citations in OpenAlex.

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  18. TheOncotarget · 2017
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  20. Potential Role of TRAIL in Metastasis of Mutant KRAS Expressing Lung Adenocarcinoma.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2016
    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

5 authors at 2 institutions in 2 countries.

Zi LiMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA.
Xiuling Xu
Lang Bai
Wenshu Chen
Yong Lin
Lovelace Respiratory Research Institute · USGuangzhou Medical University · CN

Funding

Bridging Inflammation and Cigarette Smoke-associated Lung Carcinogenesis by MUC1R01ES017328 · NIEHS · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI LIN, YONG · 2010 to 2014
$2.2M
NIEHS NIH HHS R01 ES017328NIEHS NIH HHS R01ES017328
6 · The paper itself

Abstract

Acquired chemoresistance not only blunts anticancer therapy but may also promote cancer cell migration and metastasis. Our previous studies have revealed that acquired tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resistance in lung cancer cells is associated with Akt-mediated stabilization of cellular caspase 8 and Fas-associated death domain (FADD)-like apoptosis regulator-like inhibitory protein (c-FLIP) and myeloid cell leukemia 1 (Mcl-1). In this report, we show that cells with acquired TRAIL resistance have significantly increased capacities in migration and invasion. By gene expression screening, tissue transglutaminase (TGM2) was identified as one of the genes with the highest expression increase in TRAIL-resistant cells. Suppressing TGM2 dramatically alleviated TRAIL resistance and cell migration, suggesting that TGM2 contributes to these two phenotypes in TRAIL-resistant cells. TGM2-mediated TRAIL resistance is likely through c-FLIP because TGM2 suppression significantly reduced c-FLIP but not Mcl-1 expression. The expression of matrix metalloproteinase 9 (MMP-9) was suppressed when TGM2 was inhibited, suggesting that TGM2 potentiates cell migration through up-regulating MMP-9 expression. We found that EGF receptor (EGFR) was highly active in the TRAIL-resistant cells, and suppression of EGFR dramatically reduced TGM2 expression. We further determined JNK and ERK, but not Akt and NF-κB, are responsible for EGFR-mediated TGM2 expression. These results identify a novel pathway that involves EGFR, MAPK (JNK and ERK), and TGM2 for acquired TRAIL resistance and cell migration in lung cancer cells. Because TGM2 couples TRAIL resistance and cell migration, it could be a molecular target for circumventing acquired chemoresistance and metastasis in lung cancer.

Indexed as

Gene Expression Regulation, NeoplasticCASP8 and FADD-Like Apoptosis Regulating ProteinCell Line, TumorCell MovementErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, EnzymologicGTP-Binding ProteinsHumansLung NeoplasmsMAP Kinase Kinase 4Matrix Metalloproteinase 9Protein Glutamine gamma Glutamyltransferase 2Proto-Oncogene Proteins c-aktTNF-Related Apoptosis-Inducing LigandTransglutaminasesCASP8 and FADD-Like Apoptosis Regulating ProteinErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGTP-Binding ProteinsMAP Kinase Kinase 4Matrix Metalloproteinase 9Protein Glutamine gamma Glutamyltransferase 2Proto-Oncogene Proteins c-aktTGM2 protein, humanTNF-Related Apoptosis-Inducing LigandTransglutaminasesTumor Necrosis Factor-alpha

Identifiers

PMID21525012
PMCPMC3122178
OpenAlexW2007285124

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.