Evidence map›Paper›PMID 27248176›Full record

ArticleOncotarget2016

IL-8 signaling is involved in resistance of lung carcinoma cells to erlotinib.

Romaine I Fernando, Duane H Hamilton, Charli Dominguez, Justin M David, Kristen K McCampbell, Claudia Palena

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.6field-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

41 citing papers in PubMed, 65 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Romaine I FernandoLaboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA.
Duane H HamiltonLaboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA.
Charli DominguezLaboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA.
Justin M DavidLaboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA.
Kristen K McCampbellLaboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA.
Claudia PalenaLaboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA.
National Cancer Institute · USCenter for Cancer Research · US

Funding

Novel Targets for Vaccine TherapyZICBC010937 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI PALENA, CLAUDIA · 2010 to 2022
$13.2M
6 · The paper itself

Abstract

A signaling pathway that is frequently deregulated in human carcinomas and has been explored as a therapeutic target involves the activation of the epidermal growth factor receptor (EGFR). Inhibition of EGFR via the small molecule inhibitors erlotinib and gefitinib commonly results in tumor resistance, even in patients with EGFR-mutant tumors that initially show substantial clinical responses. This study was designed to broaden our understanding of the molecular mechanisms of acquired resistance to erlotinib in lung cancer cells bearing wild type or mutated EGFR. We report here that generation of erlotinib-resistant lung cancer cells in vitro resulted in a phenotypic alteration reminiscent of an epithelial-mesenchymal transition (EMT) concomitant with a robust upregulation of the IL-8/IL-8R axis. Our results also demonstrate that upregulation of p38 MAPK signaling is responsible for the enhanced IL-8 secretion in the erlotinib-resistant tumor cells. Blockade of IL-8 signaling effectively reduced mesenchymal features of the resistant cells and also markedly enhanced their susceptibility to erlotinib. These results provide a rationale for the development of new therapeutic approaches involving blockade of IL-8 signaling for the management of acquired resistance to EGFR inhibition in patients with lung cancer.

Indexed as

Drug Resistance, NeoplasmA549 CellsAnimalsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungEpithelial-Mesenchymal TransitionErbB ReceptorsErlotinib HydrochlorideFemaleGefitinibHumansInterleukin-8Lung NeoplasmsMiceMice, NudeMutationAntineoplastic AgentsCXCL8 protein, humanEGFR protein, humanErbB ReceptorsErlotinib HydrochlorideGefitinibInterleukin-8p38 Mitogen-Activated Protein KinasesQuinazolinesepithelial-mesenchymal transitionerlotinibIL-8tumor resistance

Identifiers

PMID27248176
PMCPMC5173114
OpenAlexW2405571890

What OpenQuestion holds

Textmetadata
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.