Evidence map›Paper›PMID 29748372›Full record

ArticleCancer research2018

TRAF1 Is Critical for Regulating the BRAF/MEK/ERK Pathway in Non-Small Cell Lung Carcinogenesis.

Qiushi Wang, Ge Gao, Tianshun Zhang, Ke Yao, Hanyong Chen, Mi Hee Park, Hiroyuki Yamamoto, Keke Wang, Weiya Ma, Margarita Malakhova and 2 more

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

Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 71 citations in OpenAlex.

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  18. NMolecular cancer · 2022
    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

12 authors at 1 institution in 2 countries.

Qiushi Wang *The Hormel Institute, University of Minnesota, Austin, Minnesota.
Ge Gao *The Hormel Institute, University of Minnesota, Austin, Minnesota.
Tianshun Zhang *The Hormel Institute, University of Minnesota, Austin, Minnesota.
Ke YaoThe Hormel Institute, University of Minnesota, Austin, Minnesota.
Hanyong ChenThe Hormel Institute, University of Minnesota, Austin, Minnesota.
Mi Hee ParkThe Hormel Institute, University of Minnesota, Austin, Minnesota.
Hiroyuki YamamotoThe Hormel Institute, University of Minnesota, Austin, Minnesota.
Keke WangThe Hormel Institute, University of Minnesota, Austin, Minnesota.
Weiya MaThe Hormel Institute, University of Minnesota, Austin, Minnesota.
Margarita MalakhovaThe Hormel Institute, University of Minnesota, Austin, Minnesota.
Ann M BodeThe Hormel Institute, University of Minnesota, Austin, Minnesota.
Zigang DongThe Hormel Institute, University of Minnesota, Austin, Minnesota. zgdong@hi.umn.edu.
Hormel (United States) · US

Funding

Chemoprevention of colon cancer by targeting the Wnt/beta-catenin pathwayR01CA187027 · NCI · UNIVERSITY OF MINNESOTA · PI KANG, NINGLING, ROH, EUNMIRI · 2015 to 2019
$1.7M
Prevention of solar UV-induced skin cancer by targeting LTA4HR01CA196639 · NCI · UNIVERSITY OF MINNESOTA · PI LIU, LIANG · 2015 to 2019
$1.7M
Developing new ornithine decarboxylase inhibitors to prevent skin & colon cancerR01CA166011 · NCI · UNIVERSITY OF MINNESOTA · PI DONG, ZIGANG · 2013 to 2017
$1.6M
NCI NIH HHS R01 CA166011NCI NIH HHS R01 CA187027NCI NIH HHS R01 CA196639
6 · The paper itself

Abstract

Tumor necrosis factor receptor (TNFR)-associated factor 1 (TRAF1) is a unique TRAF protein that can interact directly or indirectly with multiple TNFR family members, regulatory proteins, kinases, and adaptors that contribute to its diverse functions in specific tissues. However, the role of TRAF1 in non-small cell lung cancer (NSCLC) remains unknown. In this study, we report that TRAF1 is overexpressed in human lung cancer cells and tissues. TRAF1 expression level inversely correlated with patient survival probability. Loss of TRAF1 decelerated tumor invasion in a urethane-induced lung carcinogenesis mouse model. Furthermore, TRAF1 expression affected TRAF2-mediated BRAF Lys48-linked ubiquitination, which was followed by the inhibition of growth and differentiation, and the induction of death in lung cancer cells. Overall, our work suggests that TRAF1 plays a novel role in the regulation of the BRAF/MEK/ERK signaling pathway in NSCLC and offers a candidate molecular target for lung cancer prevention and therapy.

Indexed as

A549 CellsAnimalsCarcinogenesisCarcinoma, Non-Small-Cell LungCell DifferentiationCell Line, TumorCell ProliferationFemaleHEK293 CellsHumansLung NeoplasmsMaleMAP Kinase Kinase KinasesMAP Kinase Signaling SystemMice, Inbred BALB CMice, KnockoutBRAF protein, humanMAP Kinase Kinase KinasesProto-Oncogene Proteins B-rafReceptors, Tumor Necrosis FactorTNF Receptor-Associated Factor 1TNF Receptor-Associated Factor 2

Identifiers

PMID29748372
PMCPMC6050072
OpenAlexW2801637031

What OpenQuestion holds

Textmetadata
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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.