Evidence map›Paper›PMID 26374334›Full record

ArticleMolecular cancer research : MCR2015

Differential IKK/NF-κB Activity Is Mediated by TSC2 through mTORC1 in PTEN-Null Prostate Cancer and Tuberous Sclerosis Complex Tumor Cells.

Yu Gao, Ronald B Gartenhaus, Rena G Lapidus, Arif Hussain, Yanting Zhang, Xinghuan Wang, Han C Dan

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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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 2 institutions in 2 countries.

Yu GaoMarlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland. Dalian Municipal Central Hospital Affiliated of Dalian Medical University, Dalian, Liaoning Province, P.R China.
Ronald B GartenhausMarlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland.
Rena G LapidusMarlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland.
Arif HussainMarlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland. Baltimore VA Medical Center, Baltimore, Maryland.
Yanting ZhangMarlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland.
Xinghuan WangDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, P.R. China.
Han C DanMarlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland. Department of Pathology, University of Maryland School of Medicine, Baltimore, Maryland. HDan@som.umaryland.edu.
University of Maryland, Baltimore · USWuhan University · CN

Funding

The Role of IKK and NF-kappaB in Controlling mTOR Signaling and TSC ProgressionR00CA149178 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI DAN, HANCAI · 2013 to 2015
$709k
The Role of IKK and NF-kappaB in Controlling mTOR Signaling and TSC ProgressionK99CA149178 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DAN, HANCAI · 2011 to 2012
$164k
NCI NIH HHS K99 CA149178NCI NIH HHS K99CA149178NCI NIH HHS R00 CA149178NCI NIH HHS R00CA149178
6 · The paper itself

Abstract

unlabelledThe serine/threonine protein kinase Akt plays a critical role in regulating proliferation, growth, and survival through phosphorylation of different downstream substrates. The mTOR is a key target for Akt to promote tumorigenesis. It has been reported that Akt activates mTOR through phosphorylation and inhibition of the tuberous sclerosis complex (TSC) protein TSC2. Previously, it was demonstrated that mTOR activates IKK/NF-κB signaling by promoting IκB kinase (IKK) activity downstream of Akt in conditions deficient of PTEN. In this study, the mechanistic role of the tumor-suppressor TSC2 was investigated in the regulation of IKK/NF-κB activity in PTEN-null prostate cancer and in TSC2-mutated tumor cells. The results demonstrate that TSC2 inhibits IKK/NF-κB activity downstream of Akt and upstream of mTORC1 in a PTEN-deficient environment. However, TSC2 promotes IKK/NF-κB activity upstream of Akt and mTORC1 in TSC2 mutated tumor cells. These data indicate that TSC2 negatively or positively regulates IKK/NF-κB activity in a context-dependent manner depending on the genetic background. IMPLICATIONS: This study provides fundamental insight for understanding the molecular details by which TSC2/mTOR regulates NF-κB signaling in different tumors.

Indexed as

Cell Line, TumorGene Expression Regulation, NeoplasticHeLa CellsHumansI-kappa B KinaseMaleMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesMutationNF-kappa BProstatic NeoplasmsPTEN PhosphohydrolaseSignal TransductionTOR Serine-Threonine KinasesTuberous SclerosisTuberous Sclerosis Complex 2 ProteinI-kappa B KinaseMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesNF-kappa BPTEN PhosphohydrolasePTEN protein, humanTOR Serine-Threonine KinasesTSC2 protein, humanTuberous Sclerosis Complex 2 ProteinTumor Suppressor Proteins

Identifiers

PMID26374334
PMCPMC4690470
OpenAlexW2180010206

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.