Evidence map›Paper›PMID 31491919›Full record

ReviewInternational journal of molecular sciences2019

Dual role of Endoplasmic Reticulum Stress-Mediated Unfolded Protein Response Signaling Pathway in Carcinogenesis.

Natalia Siwecka, Wioletta Rozpędek, Dariusz Pytel, Adam Wawrzynkiewicz, Adam Dziki, Łukasz Dziki, J Alan Diehl, Ireneusz Majsterek

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
–field-weighted citation impact
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

101 citing papers in PubMed.

  1. Review
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  8. International journal of molecular sciences · 2026
    Article
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  15. Review
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41 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

8 authors.

Natalia SiweckaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 90-419 Lodz, Poland. natalia.siwecka@stud.umed.lodz.pl.
Wioletta RozpędekDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 90-419 Lodz, Poland. wioletta.rozpedek@umed.lodz.pl.
Dariusz PytelDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA. pytel@musc.edu.
Adam WawrzynkiewiczDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 90-419 Lodz, Poland. adam.wawrzynkiewicz@stud.umed.lodz.pl.
Adam DzikiDepartment of General and Colorectal Surgery, Medical University of Lodz, 90-419 Lodz, Poland. adam.dziki@umed.lodz.pl.
Łukasz DzikiDepartment of General and Colorectal Surgery, Medical University of Lodz, 90-419 Lodz, Poland. lukasz.dziki@umed.lodz.pl.
J Alan DiehlDepartment of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA. diehl@musc.edu.
Ireneusz MajsterekDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 90-419 Lodz, Poland. ireneusz.majsterek@umed.lodz.pl.

Funding

UPR, interferon signaling and tumorigenesisP01CA165997 · NCI · UNIVERSITY OF PENNSYLVANIA · PI DIEHL, JOHN ALAN · 2013 to 2023
$10.9M
Narodowe Centrum Nauki 2015/19/N/NZ3/00055Narodowe Centrum Nauki 2016/23/B/NZ5/02630NCI NIH HHS P01 CA165997Uniwersytet Medyczny w Lodzi 502-03/5-108-05/502-54-224-18
6 · The paper itself

Abstract

Cancer constitutes a grave problem nowadays in view of the fact that it has become one of the main causes of death worldwide. Poor clinical prognosis is presumably due to cancer cells metabolism as tumor microenvironment is affected by oxidative stress. This event triggers adequate cellular response and thereby creates appropriate conditions for further cancer progression. Endoplasmic reticulum (ER) stress occurs when the balance between an ability of the ER to fold and transfer proteins and the degradation of the misfolded ones become distorted. Since ER is an organelle relatively sensitive to oxidative damage, aforementioned conditions swiftly cause the activation of the unfolded protein response (UPR) signaling pathway. The output of the UPR, depending on numerous factors, may vary and switch between the pro-survival and the pro-apoptotic branch, and hence it displays opposing effects in deciding the fate of the cancer cell. The role of UPR-related proteins in tumorigenesis, such as binding the immunoglobulin protein (BiP) and inositol-requiring enzyme-1α (IRE1α), activating transcription factor 6 (ATF6) or the protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), has already been specifically described so far. Nevertheless, due to the paradoxical outcomes of the UPR activation as well as gaps in current knowledge, it still needs to be further investigated. Herein we would like to elicit the actual link between neoplastic diseases and the UPR signaling pathway, considering its major branches and discussing its potential use in the development of a novel, anti-cancer, targeted therapy.

Indexed as

Endoplasmic Reticulum StressSignal TransductionUnfolded Protein ResponseAnimalsApoptosisBiomarkers, TumorCell Transformation, NeoplasticDisease ProgressionDisease SusceptibilityEndoplasmic ReticulumHumansNeoplasmsReactive Oxygen SpeciesBiomarkers, TumorReactive Oxygen Speciesapoptosiscancercancer treatmentcarcinogenesisendoplasmic reticulum stressprotein kinase R (PKR)-like endoplasmic reticulum kinase (PERK)reactive oxygen speciesunfolded protein response

Identifiers

PMID31491919
PMCPMC6770252

What OpenQuestion holds

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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.