Evidence map›Paper›PMID 21217782›Full record

ArticleOncogene2011

LITAF and TNFSF15, two downstream targets of AMPK, exert inhibitory effects on tumor growth.

J Zhou, Z Yang, T Tsuji, J Gong, J Xie, C Chen, W Li, S Amar, Z Luo

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Polymorphism rs6478109 in theThe Journal of international medical research · 2020
    Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. TNFSF15 facilitates the differentiation of CD11bCancer biology & medicine · 2023
    Article
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  10. Review
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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

9 authors at 4 institutions in 2 countries.

J ZhouDepartment of Biochemistry, Boston University School of Medicine, Boston, MA 02118, USA.
Z Yang
T Tsuji
J Gong
J Xie
C Chen
W Li
S Amar
Z Luo
Boston University · USBeth Israel Deaconess Medical Center · USHarvard University · USShaanxi Normal University · CN

Funding

Role of LITAF in Inflammatory ProcessesR01DE014079 · NIDCR · NEW YORK MEDICAL COLLEGE · PI AMAR, SALOMON · 2002 to 2016
$5.4M
Lung Lysyl Oxidase Regulation by Metal Ion HomeostasisR01ES011340 · NIEHS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LI, WANDE · 2003 to 2013
$3.2M
Role of Nicotine in Lung CarcinogenesisR01CA124490 · NCI · NORTHEASTERN UNIVERSITY · PI CHEN, CHANGYAN · 2007 to 2011
$1.6M
The fuel sensing enzyme AMPK in the pathogenesis of prostate cancerR01CA118918 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LUO, ZHIJUN · 2006 to 2010
$1.1M
NCI NIH HHS CA124490NCI NIH HHS R01 CA118918NCI NIH HHS R01 CA124490NIDCR NIH HHS R01 DE014079NIEHS NIH HHS R01 ES011340
6 · The paper itself

Abstract

Lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF) α factor (LITAF) is a multiple functional molecule whose sequence is identical to the small integral membrane protein of the lysosome/late endosome. LITAF was initially identified as a transcription factor that activates transcription of proinflammatory cytokine in macrophages in response to LPS. Mutations of the LITAF gene are associated with a genetic disease, called Charcot-Marie-Tooth syndrome. Recently, we have reported that mRNA levels of LITAF and TNF superfamily member 15 (TNFSF15) are upregulated by 5' adenosine monophosphate (AMP)-activated protein kinase (AMPK). The present study further assesses their biological functions. Thus, we show that 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), a pharmacological activator of AMPK, increases the abundance of LITAF and TNFSF15 in LNCaP and C4-2 prostate cancer cells, which is abrogated by small hairpin RNA (shRNA) or the dominant-negative mutant of AMPK α1 subunit. Our data further demonstrate that AMPK activation upregulates the transcription of LITAF. Intriguingly, silencing LITAF by shRNA enhances proliferation, anchorage-independent growth of these cancer cells and tumor growth in the xenograft model. In addition, our study reveals that LITAF mediates the effect of AMPK by binding to a specific sequence in the promoter region. Furthermore, we show that TNFSF15 remarkably inhibits the growth of prostate cancer cells and bovine aortic endothelial cells in vitro, with a more potent effect toward the latter. In conjuncture, intratumoral injection of TNFSF15 significantly reduces the size of tumors and number of blood vessels and induces changes that are characteristic of tumor cell differentiation. Therefore, our studies for the first time establish the regulatory axis of AMPK-LITAF-TNFSF15 and also suggest that LITAF may function as a tumor suppressor.

Indexed as

Adenylate KinaseEnzyme ActivationHumansNeoplasmsNeovascularization, PathologicNuclear ProteinsTranscription FactorsTumor Necrosis Factor Ligand Superfamily Member 15Adenylate KinaseLITAF protein, humanNuclear ProteinsTNFSF15 protein, humanTranscription FactorsTumor Necrosis Factor Ligand Superfamily Member 15

Identifiers

PMID21217782
PMCPMC3431012
OpenAlexW1966634911

What OpenQuestion holds

Textmetadata
LicenceTDM
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.