Evidence map›Paper›PMID 24154876›Full record

ArticleCancer research2013

TRAF4 is a critical molecule for Akt activation in lung cancer.

Wei Li, Cong Peng, Mee-Hyun Lee, DoYoung Lim, Feng Zhu, Yang Fu, Ge Yang, Yuqiao Sheng, Lanbo Xiao, Xin Dong and 4 more

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

78 citing papers in PubMed, 116 citations in OpenAlex.

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  19. TRAF4-mediated nonproteolytic ubiquitination of androgen receptor promotes castration-resistant prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. Article

18 more citing papers are in PubMed but not listed here.

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

14 authors at 4 institutions in 3 countries.

Wei LiAuthors' Affiliations: The Hormel Institute, University of Minnesota, Austin, Minnesota; Cancer Research Institute, Xiangya School of Medicine; Xiangya Hospital, Central South University, Changsha, Hunan; The First Affiliated Hospital; and Physiology and Pathophysiology, Basic Medical School, Zhengzhou University, Zhengzhou, Henan, China.
Cong Peng
Mee-Hyun Lee
DoYoung Lim
Feng Zhu
Yang Fu
Ge Yang
Yuqiao Sheng
Lanbo Xiao
Xin Dong
WeiYa Ma
Ann M Bode
Ya Cao
Zigang Dong
Zhengzhou University · CNXiangya Hospital Central South University · CNCentral South University · CNCancer Research Institute of the Slovak Academy of Sciences · SK

Funding

Anticarcinogenic Mechanisms of Tea ConstituentsR01CA081064 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI DONG, ZIGANG · 1999 to 2007
$1.9M
The role of histone phosphorylation in arsenic-induced cell transformation and skR01ES016548 · NIEHS · UNIVERSITY OF MINNESOTA · PI DONG, ZIGANG · 2008 to 2012
$1.7M
Anticarcinogenic Mechanisms of Tea ConstituentsR37CA081064 · NCI · UNIVERSITY OF MINNESOTA · PI DONG, ZIGANG · 2008 to 2012
$1.5M
Inhibition of Carcinogenesis by Tea and Tea ConstituentsR01CA120388 · NCI · UNIVERSITY OF MINNESOTA · PI DONG, ZIGANG · 2006 to 2010
$1.3M
NCI NIH HHS CA081064NCI NIH HHS CA120388NCI NIH HHS R01 CA081064NCI NIH HHS R01 CA120388NCI NIH HHS R37 CA081064NIEHS NIH HHS ES016548NIEHS NIH HHS R01 ES016548
6 · The paper itself

Abstract

TRAF4 is an adapter protein overexpressed in certain cancers, but its contributions to tumorigenesis are unclear. In lung cancer cells and primary lung tumors, we found that TRAF4 is overexpressed. RNA interference-mediated attenuation of TRAF4 expression blunted the malignant phenotype in this setting, exerting inhibitory effects on cell proliferation, anchorage-independent growth, and tumor development in a xenograft mouse model. Unexpectedly, we discovered that TRAF4, but not Skp2, was required for activation of the pivotal cell survival kinase Akt through ubiquitination. Furthermore, TRAF4 attenuation impaired glucose metabolism by inhibiting expression of Glut1 and HK2 mediated by the Akt pathway. Overall, our work suggests that TRAF4 offers a candidate molecular target for lung cancer prevention and therapy.

Indexed as

AdenocarcinomaAnimalsCarcinoma, Squamous CellCells, CulturedEnzyme ActivationGene Expression Regulation, NeoplasticHumansLung NeoplasmsMiceMice, NudeNIH 3T3 CellsOncogene Protein v-aktRNA, Small InterferingTNF Receptor-Associated Factor 4Xenograft Model Antitumor AssaysOncogene Protein v-aktRNA, Small InterferingTNF Receptor-Associated Factor 4TRAF4 protein, human

Identifiers

PMID24154876
PMCPMC3856436
OpenAlexW2171239378

What OpenQuestion holds

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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.