Evidence map›Paper›PMID 26343532›Full record

ArticleScientific reports2015

LAPTM4B is associated with poor prognosis in NSCLC and promotes the NRF2-mediated stress response pathway in lung cancer cells.

Yuho Maki, Junya Fujimoto, Wenhua Lang, Li Xu, Carmen Behrens, Ignacio I Wistuba, Humam Kadara

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. 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
3.6field-weighted citation impact, top 8% 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, 22 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

7 authors at 1 institution in 1 country.

Yuho MakiDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, U.S.A.
Junya FujimotoDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, U.S.A.
Wenhua LangDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, U.S.A.
Li XuDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, U.S.A.
Carmen BehrensDepartment of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, U.S.A.
Ignacio I WistubaDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, U.S.A.
Humam KadaraDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, U.S.A.
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
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
NCI NIH HHS CA16672NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA070907NCI NIH HHS P50 CA70907
6 · The paper itself

Abstract

We recently demonstrated that lysosomal protein transmembrane 4 beta (LAPTM4B) is elevated in non-small cell lung cancers (NSCLCs) and in the surrounding premalignant airway field of cancerization. In the present study, we sought to begin to understand the relevance of LAPTM4B expression and signaling to NSCLC pathogenesis. In situ hybridization analysis of LAPTM4B transcript in tissue microarrays comprised of 368 NSCLCs demonstrated that LAPTM4B expression was significantly increased in smoker compared to non-smoker lung adenocarcinoma tumors (P < 0.001) and was significantly associated with poor overall survival (P < 0.05) in adenocarcinoma patients. Knockdown of LAPTM4B expression inhibited cell growth, induced cellular apoptosis and decreased cellular autophagy in serum starved lung cancer cells. Expression profiling coupled with pathways analysis revealed decreased activation of the nuclear factor erythroid 2-like 2 (NRF2) stress response pathway following LAPTM4B knockdown. Further analysis demonstrated that LAPTM4B augmented the expression and nuclear translocation of the NRF2 transcription factor following serum deprivation as well as increased the expression of NRF2 target genes such as heme oxygenase 1/HMOX1). Our study points to the relevance of LAPTM4B expression to NSCLC pathogenesis as well as to the probable role of LAPTM4B/NRF2 signaling in promoting lung cancer cell survival.

Indexed as

Signal TransductionStress, PhysiologicalActive Transport, Cell NucleusAutophagyCarcinoma, Non-Small-Cell LungCluster AnalysisGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLung NeoplasmsMembrane ProteinsNF-E2-Related Factor 2Oncogene ProteinsPrognosisProtein TransportLAPTM4B protein, humanMembrane ProteinsNF-E2-Related Factor 2Oncogene Proteins

Identifiers

PMID26343532
PMCPMC4561374
OpenAlexW2129762266

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.