Evidence map›Paper›PMID 24496235›Full record

ArticleThe Journal of investigative dermatology2014

Stat3 binds to mtDNA and regulates mitochondrial gene expression in keratinocytes.

Everardo Macias, Dharanija Rao, Steve Carbajal, Kaoru Kiguchi, John DiGiovanni

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
3.0field-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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 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

5 authors at 1 institution in 1 country.

Everardo MaciasDivision of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, Texas, USA.
Dharanija RaoDivision of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, Texas, USA.
Steve CarbajalDivision of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, Texas, USA.
Kaoru KiguchiDivision of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, Texas, USA.
John DiGiovanniDivision of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, Texas, USA; Department of Nutritional Sciences, College of Natural Sciences, The University of Texas at Austin, Austin, Texas, USA. Electronic address: john.digiovanni@austin.utexas.edu.
The University of Texas at Austin · US

Funding

TYROSINE KINASES AND C SRC IN SKIN CANCERR01CA076520 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DIGIOVANNI, JOHN · 1998 to 2012
$3.7M
NCI NIH HHS R01 CA076520
6 · The paper itself

Abstract

The nuclear transcription factor signal transducer and activator of transcription 3 (Stat3) has recently been reported to have a localized mitochondrial regulatory function. Current data suggest that mitochondrial Stat3 (mitoStat3) is necessary for maximal mitochondrial activity and for Ras-mediated transformation independent of Stat3 nuclear activity. We have previously shown that Stat3 has a pivotal role in epithelial carcinogenesis. Therefore, the aim of the current study was to determine the role of mitoStat3 in epidermal keratinocytes. Herein, we show that normal and neoplastic keratinocytes contain a pool of mitoStat3. EGF and 12-O-tetradecanoylphorbol-13-acetate induce Stat3 mitochondrial translocation mediated through the phosphorylation of Stat3 at Ser727. In addition, we report that mitoStat3 binds mtDNA and associates with the mitochondrial transcription factor A. Furthermore, Stat3 ablation resulted in an increase of mitochondrial-encoded gene transcripts. An increase in key nuclear-encoded metabolic genes, PGC-1α and NRF-1, was also observed in Stat3-null keratinocytes; however, no changes in nuclear-encoded electron transport chain gene transcripts or mtDNA copy number were observed. Collectively, our findings suggest a heretofore-unreported function for mitoStat3 as a potential mitochondrial transcription factor in keratinocytes. This mitoStat3-mtDNA interaction may represent an alternate signaling pathway that could alter mitochondrial function and biogenesis and have a role in tumorigenesis.

Indexed as

AnimalsCell Transformation, NeoplasticDNA, MitochondrialEpidermal CellsEpidermisGene ExpressionHumansKeratinocytesMiceMitochondriaPrimary Cell CultureSignal TransductionSkin NeoplasmsSTAT3 Transcription FactorDNA, MitochondrialSTAT3 protein, humanStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID24496235
PMCPMC4057971
OpenAlexW2030456165

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.