Evidence map›Paper›PMID 28186986›Full record

ArticleOncotarget2017

Common cytotoxic chemotherapeutics induce epithelial-mesenchymal transition (EMT) downstream of ER stress.

Parag P Shah, Tess V Dupre, Leah J Siskind, Levi J Beverly

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.7field-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

33 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Multidrug Resistance: Are We Still Afraid of the Big Bad Wolf.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
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  8. Article
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  12. Article
  13. The Hallmarks of Cancer as Ecologically Driven Phenotypes.Frontiers in ecology and evolution · 2021
    Article
  14. Review
  15. [A Review of the Roles of Endoplasmic Reticulum Stress in Cancer Cell Metastasis].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021
    Review
  16. Review
  17. Review
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  19. Article
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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

4 authors at 2 institutions in 1 country.

Parag P ShahJames Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202, USA.
Tess V DupreDepartment of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Leah J SiskindDepartment of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Levi J BeverlyJames Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202, USA.
University of Louisville · USJames Graham Brown Foundation · US

Funding

Ubiquilins regulate EMT, migration and invasion of human lung cancerR01CA193220 · NCI · UNIVERSITY OF LOUISVILLE · PI BEVERLY, LEVI J · 2015 to 2019
$2.3M
Molecular Targets COBREP20GM103482 · NIGMS · UNIVERSITY OF LOUISVILLE · PI MILLER, DONALD M. · 2012 to 2012
$2.0M
Role of Ceramide-induced Kidney Cell Death in Acute Kidney InjuryR01DK093462 · NIDDK · UNIVERSITY OF LOUISVILLE · PI SISKIND, LEAH J · 2012 to 2016
$1.6M
NCI NIH HHS R01 CA193220NIDDK NIH HHS R01 DK093462NIGMS NIH HHS P20 GM103482
6 · The paper itself

Abstract

Endoplasmic reticulum (ER) in eukaryotes is a main organelle involved in a wide variety of functions including calcium storage, lipid biosynthesis, protein folding and protein transport. Disruption of ER homeostasis leads to ER stress and activation of the unfolded protein response (UPR). We and others have previously found that ER stress induces EMT in different cellular systems. Induction of ER stress with chemical modulators of ER homeostasis was sufficient to activate an EMT-like state in all cellular systems tested. Here, we provide evidence for the first time demonstrating that ER stress induces EMT that is neither cancer cell specific nor cell-type specific. In addition, we observed that chemotherapeutic drugs commonly used to treat patients also activate ER stress that is concomitant with activation of an EMT-like state. Interestingly, we find that following removal of ER stress, partial EMT characteristics still persist indicating that ER stress induced EMT is a long-term effect. Induction of mesenchymal characteristics, following chemotherapeutics treatment may be involved in providing cancer stemness and invasiveness in the cellular system. Interestingly, we find that mice treated with cisplatin have elevated level of ER stress and EMT markers in multiple tissues including lung, liver and kidneys. Furthermore, increased ER stress, as demonstrated by increased Bip, Chop, PDI, Ero1α and IRE1, and EMT, as demonstrated by increased Vimentin and Snail, is a hallmark of primary lung adenocarcinoma samples from patients. These observations have potential clinical relevance because overexpression of ER stress and EMT markers might contribute to chemoresistance and poor survival of lung adenocarcinoma patients.

Indexed as

AdenocarcinomaAnimalsAntineoplastic AgentsApoptosisBiomarkers, TumorCell MovementCell ProliferationEndoplasmic ReticulumEndoplasmic Reticulum StressEpithelial-Mesenchymal TransitionHumansLung NeoplasmsMaleMiceMice, Inbred C57BLNeoplasm MetastasisAntineoplastic AgentsBiomarkers, TumorchemotherapeuticsEMTER stressinvasionmigration

Identifiers

PMID28186986
PMCPMC5410250
OpenAlexW2587264845

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.