Evidence map›Paper›PMID 27459239›Full record

ArticleAutophagy2016

Role for DUSP1 (dual-specificity protein phosphatase 1) in the regulation of autophagy.

Juan Wang, Jun-Ying Zhou, Dhonghyo Kho, John J Reiners, Gen Sheng Wu

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
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  5. The ATG14: multi-layer autophagy control and an emerging therapeutic target in cancer.Apoptosis : an international journal on programmed cell death · 2026
    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

5 authors at 2 institutions in 1 country.

Juan Wanga Molecular Therapeutics Program , Karmanos Cancer Institute, Wayne State University School of Medicine , Detroit , MI , USA.
Jun-Ying Zhoua Molecular Therapeutics Program , Karmanos Cancer Institute, Wayne State University School of Medicine , Detroit , MI , USA.
Dhonghyo Khoa Molecular Therapeutics Program , Karmanos Cancer Institute, Wayne State University School of Medicine , Detroit , MI , USA.
John J Reinersa Molecular Therapeutics Program , Karmanos Cancer Institute, Wayne State University School of Medicine , Detroit , MI , USA.
Gen Sheng Wua Molecular Therapeutics Program , Karmanos Cancer Institute, Wayne State University School of Medicine , Detroit , MI , USA.
Wayne State University · USThe Barbara Ann Karmanos Cancer Institute · US

Funding

A novel role for PARP1 in regulation of autophagyR21CA178111 · NCI · WAYNE STATE UNIVERSITY · PI WU, GEN SHENG · 2013 to 2014
$358k
NCI NIH HHS R21 CA178111
6 · The paper itself

Abstract

Accumulating evidence suggests that mitogen-activated protein kinases (MAPKs) regulate macroautophagy/autophagy. However, the involvement of dual-specificity protein phosphatases (DUSPs), endogenous inhibitors for MAPKs, in autophagy remains to be determined. Here we report that DUSP1/MKP-1, the founding member of the DUSP family, plays a critical role in regulating autophagy. Specifically, we demonstrate that DUSP1 knockdown by shRNA in human ovarian cancer CAOV3 cells and knockout in murine embryonic fibroblasts, increases both basal and rapamycin-increased autophagic flux. Overexpression of DUSP1 had the opposite effect. Importantly, knockout of Dusp1 promoted phosphorylation of ULK1 at Ser555, and BECN1/Beclin 1 at Ser15, and the association of PIK3C3/VPS34, ATG14, BECN1 and MAPK, leading to the activation of the autophagosome-initiating class III phosphatidylinositol 3-kinase (PtdIns3K) complex. Furthermore, knockdown and pharmacological inhibitor studies indicated that DUSP1-mediated suppression of autophagy reflected inactivation of the MAPK1-MAPK3 members of the MAPK family. Knockdown of DUSP1 sensitized CAOV3 cells to rapamycin-induced antigrowth activity. Moreover, CAOV3-CR cells, a line that had acquired cisplatin resistance, exhibited an elevated DUSP1 level and were refractory to rapamycin-induced autophagy and cytostatic effects. Knockdown of DUSP1 in CAOV3-CR cells restored sensitivity to rapamycin. Collectively, this work identifies a previously unrecognized role for DUSP1 in regulating autophagy and suggests that suppression of DUSP1 may enhance the therapeutic activity of rapamycin.

Indexed as

AutophagyAnimalsAutophagosomesCell Line, TumorCisplatinDrug Resistance, NeoplasmDual Specificity Phosphatase 1Extracellular Signal-Regulated MAP KinasesFemaleGene Knockdown TechniquesHumansMiceMice, KnockoutMultiprotein ComplexesOvarian NeoplasmsSequestosome-1 ProteinCisplatinDual Specificity Phosphatase 1Dusp1 protein, mouseExtracellular Signal-Regulated MAP KinasesMultiprotein ComplexesSequestosome-1 ProteinSirolimusSqstm1 protein, mouseautophagycisplatin resistanceDUSP1MAPK/ERKovarian cancer

Identifiers

PMID27459239
PMCPMC5079544
OpenAlexW2487234715

What OpenQuestion holds

Textmetadata
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.