Evidence map›Paper›PMID 25951043›Full record

ReviewAutophagy2015

The role of STAT3 in autophagy.

Liangkun You, Zhanggui Wang, Hongsen Li, Jiawei Shou, Zhao Jing, Jiansheng Xie, Xinbing Sui, Hongming Pan, Weidong Han

Open access · hybridAbstract readReview
In one paragraph

Review in Autophagy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 294 papers.

0numbers the graph read from it
0cells of the map it votes in
294citing papers in PubMed
14.8field-weighted citation impact, top 1% 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

294 citing papers in PubMed, 521 citations in OpenAlex.

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234 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

9 authors at 4 institutions in 1 country.

Liangkun Youa Department of Medical Oncology; Zhejiang University ; Hangzhou , Zhejiang , China.
Zhanggui Wang
Hongsen Li
Jiawei Shou
Zhao Jing
Jiansheng Xie
Xinbing Sui
Hongming Pan
Weidong Han
Indiana University School of MedicineSir Run Run Shaw Hospital · CNZhejiang University · CNState Key Laboratory of Cancer Biology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an evolutionarily conserved process in eukaryotes that eliminates harmful components and maintains cellular homeostasis in response to a series of extracellular insults. However, these insults may trigger the downstream signaling of another prominent stress responsive pathway, the STAT3 signaling pathway, which has been implicated in multiple aspects of the autophagic process. Recent reports further indicate that different subcellular localization patterns of STAT3 affect autophagy in various ways. For example, nuclear STAT3 fine-tunes autophagy via the transcriptional regulation of several autophagy-related genes such as BCL2 family members, BECN1, PIK3C3, CTSB, CTSL, PIK3R1, HIF1A, BNIP3, and microRNAs with targets of autophagy modulators. Cytoplasmic STAT3 constitutively inhibits autophagy by sequestering EIF2AK2 as well as by interacting with other autophagy-related signaling molecules such as FOXO1 and FOXO3. Additionally, the mitochondrial translocation of STAT3 suppresses autophagy induced by oxidative stress and may effectively preserve mitochondria from being degraded by mitophagy. Understanding the role of STAT3 signaling in the regulation of autophagy may provide insight into the classic autophagy model and also into cancer therapy, especially for the emerging targeted therapy, because a series of targeted agents execute antitumor activities via blocking STAT3 signaling, which inevitably affects the autophagy pathway. Here, we review several of the representative studies and the current understanding in this particular field.

Indexed as

AutophagyAnimalsHumansMitochondriaModels, BiologicalNeoplasmsSTAT3 Transcription FactorSubcellular FractionsSTAT3 Transcription FactorALK, anaplastic lymphoma receptor tyrosine kinaseATF4, activating transcription factor 4autophagyBNIP3, BCL2/adenovirus E1B 19kDa interacting protein 3cancerCNTF, ciliary neurotrophic factorConA, concanavalin ACOX8, cytochrome c oxidase subunit VIIICTSB, cathepsin BCTSL, cathepsin LCuB, cucurbitacin BCYCS, cytochrome c, somaticEGF, epidermal growth factorEIF2A, eukaryotic initiation factor 2A, 65kDaEIF2AK2, eukaryotic translation initiation factor 2-α kinase 2ER, endoplasmic reticulumETC, electron transport chainFOXO1/3, forkhead box O1/3HDAC3, histone deacetylase 3HIF1A, hypoxia inducible factor 1, α subunit (basic helix-loop-helix transcription factor)IL6, interleukin 6IMM, inner mitochondrial membraneKDR, kinase insert domain receptorLMP, lysosomal membrane permeabilizationMAP1LC3A, microtubule-associated protein 1 light chain 3 αMAPK1, mitogen-activated protein kinase 1miRNA, microRNAmitophagymitoSTAT3, mitochondrial STAT3MLS, mitochondrial localization sequenceMMP14, matrix metallopeptidase 14 (membrane-inserted)NDUFA13, NADH dehydrogenase (ubiquinone) 1 α subcomplex, 13NES, nuclear export signalNFKB1, nuclear factor of kappa light polypeptide gene enhancer in B-cells 1NLS, nuclear localization signalPDGFRB, platelet-derived growth factor receptor, β polypeptidePRKAA2, protein kinase, AMP-activated, α 2 catalytic subunitPTPN11, protein tyrosine phosphatase, non-receptor type 11PTPN2, protein tyrosine phosphatase, non-receptor type 2PTPN6, protein tyrosine phosphatase, non-receptor type 6receptor tyrosine kinasesROS, reactive oxygen speciesRTK, receptor tyrosine kinasesSH2, src homology 2STAT3STAT3, signal transducer and activator of transcription 3 (acute-phase response factor)targeted therapyVHL, von Hippel-Lindau tumor suppressor, E3 ubiquitin protein ligaseXPO1, exportin 1

Identifiers

PMID25951043
PMCPMC4509450
OpenAlexW1853894947

What OpenQuestion holds

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LicenceCC BY-NC
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.