Evidence map›Paper›PMID 26513173›Full record

ArticleOncotarget2015

Depletion of the thiol oxidoreductase ERp57 in tumor cells inhibits proliferation and increases sensitivity to ionizing radiation and chemotherapeutics.

Melanie Hussmann, Kirsten Janke, Philip Kranz, Fabian Neumann, Evgenija Mersch, Melanie Baumann, Kirsten Goepelt, Ulf Brockmeier, Eric Metzen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Exploring druggable targets and inflammation-mediated pathways in cancer: a Mendelian randomization analysis integrating transcriptomic and proteomic data.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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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 1 institution in 1 country.

Melanie HussmannInstitut für Physiologie, Universität Duisburg-Essen, D45122 Essen, Germany.
Kirsten JankeInstitut für Physiologie, Universität Duisburg-Essen, D45122 Essen, Germany.
Philip KranzInstitut für Physiologie, Universität Duisburg-Essen, D45122 Essen, Germany.
Fabian NeumannInstitut für Physiologie, Universität Duisburg-Essen, D45122 Essen, Germany.
Evgenija MerschInstitut für Physiologie, Universität Duisburg-Essen, D45122 Essen, Germany.
Melanie BaumannInstitut für Physiologie, Universität Duisburg-Essen, D45122 Essen, Germany.
Kirsten GoepeltInstitut für Physiologie, Universität Duisburg-Essen, D45122 Essen, Germany.
Ulf BrockmeierInstitut für Physiologie, Universität Duisburg-Essen, D45122 Essen, Germany.
Eric MetzenInstitut für Physiologie, Universität Duisburg-Essen, D45122 Essen, Germany.
University of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rapidly growing tumor cells must synthesize proteins at a high rate and therefore depend on an efficient folding and quality control system for nascent secretory proteins in the endoplasmic reticulum (ER). The ER resident thiol oxidoreductase ERp57 plays an important role in disulfide bond formation. Lentiviral, doxycycline-inducible ERp57 knockdown was combined with irradiation and treatment with chemotherapeutic agents. The knockdown of ERp57 significantly enhanced the apoptotic response to anticancer treatment in HCT116 colon cancer cells via a p53-dependent mechanism. Instead of a direct interaction with p53, depletion of ERp57 induced cell death via a selective activation of the PERK branch of the Unfolded Protein Response (UPR). In contrast, apoptosis was reduced in MDA-MB-231 breast cancer cells harboring mutant p53. Nevertheless, we observed a strong reduction of proliferation in response to ERp57 knockdown in both cell lines regardless of the p53 status. Depletion of ERp57 reduced the phosphorylation activity of the mTOR-complex1 (mTORC1) as demonstrated by reduction of p70S6K phosphorylation. Our data demonstrate that ERp57 is a promising target for anticancer therapy due to synergistic p53-dependent induction of apoptosis and p53-independent inhibition of proliferation.

Indexed as

ApoptosisBreast NeoplasmsCell Line, TumorCell ProliferationColonic NeoplasmsEndoplasmic ReticulumGene Knockdown TechniquesHCT116 CellsHEK293 CellsHumansProtein Disulfide-IsomerasesRadiation, IonizingTumor Suppressor Protein p53Unfolded Protein ResponsePDIA3 protein, humanProtein Disulfide-IsomerasesTumor Suppressor Protein p53apoptosisendoplasmic reticulumER chaperonep53unfolded protein response

Identifiers

PMID26513173
PMCPMC4770770
OpenAlexW1851397458

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.