Evidence map›Paper›PMID 32503307›Full record

ReviewInternational journal of molecular sciences2020

Association of the Epithelial-Mesenchymal Transition (EMT) with Cisplatin Resistance.

Milad Ashrafizadeh, Ali Zarrabi, Kiavash Hushmandi, Mahshad Kalantari, Reza Mohammadinejad, Tahereh Javaheri, Gautam Sethi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed
13.8field-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

126 citing papers in PubMed, 242 citations in OpenAlex.

  1. Article
  2. Review
  3. Translational cancer research · 2026
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  9. Programmed cell death in triple-negative breast cancer.Cellular & molecular biology letters · 2025
    Review
  10. Article
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  18. Overexpression ofOncology letters · 2025
    Article
  19. Article
  20. Article

66 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

7 authors at 7 institutions in 4 countries.

Milad AshrafizadehDepartment of Basic Science, Faculty of Veterinary Medicine, University of Tabriz, Tabriz 5166616471, Iran.
Ali ZarrabiSabanci University Nanotechnology Research and Application Center (SUNUM), Tuzla, Istanbul 34956, Turkey.
Kiavash HushmandiDepartment of Food Hygiene and Quality Control, Division of Epidemiology, Faculty of Veterinary Medicine, University of Tehran, Tehran 1417414418, Iran.
Mahshad KalantariDepartment of Genetic Science, Tehran Medical Science Branch, Islamic Azad University, Tehran 19168931813, Iran.
Reza MohammadinejadPharmaceutics Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman 1355576169, Iran.
Tahereh JavaheriHealth Informatics Lab, Metropolitan College, Boston University, Boston, MA 02215, USA.
Gautam SethiDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117600, Singapore.
Boston University · USIslamic Azad University Medical Branch of Tehran · IRKerman University of Medical Sciences · IRNational University of Singapore · SGSabancı Üniversitesi · TRShiraz University of Medical Sciences · IRUniversity of Tabriz · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Therapy resistance is a characteristic of cancer cells that significantly reduces the effectiveness of drugs. Despite the popularity of cisplatin (CP) as a chemotherapeutic agent, which is widely used in the treatment of various types of cancer, resistance of cancer cells to CP chemotherapy has been extensively observed. Among various reported mechanism(s), the epithelial-mesenchymal transition (EMT) process can significantly contribute to chemoresistance by converting the motionless epithelial cells into mobile mesenchymal cells and altering cell-cell adhesion as well as the cellular extracellular matrix, leading to invasion of tumor cells. By analyzing the impact of the different molecular pathways such as microRNAs, long non-coding RNAs, nuclear factor-κB (NF-ĸB), phosphoinositide 3-kinase-related protein kinase (PI3K)/Akt, mammalian target rapamycin (mTOR), and Wnt, which play an important role in resistance exhibited to CP therapy, we first give an introduction about the EMT mechanism and its role in drug resistance. We then focus specifically on the molecular pathways involved in drug resistance and the pharmacological strategies that can be used to mitigate this resistance. Overall, we highlight the various targeted signaling pathways that could be considered in future studies to pave the way for the inhibition of EMT-mediated resistance displayed by tumor cells in response to CP exposure.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsCell DifferentiationCisplatinEpithelial-Mesenchymal TransitionForkhead Box Protein O1HumansMicroRNAsNeoplasmsNF-kappa BPhosphatidylinositol 3-KinasesSignal TransductionTOR Serine-Threonine KinasesAntineoplastic AgentsCisplatinForkhead Box Protein O1FOXO1 protein, humanMicroRNAsMTOR protein, humanNF-kappa BPhosphatidylinositol 3-KinasesTOR Serine-Threonine Kinasescancer therapychemoresistancecisplatinepithelial–mesenchymal transition (EMT)signal transduction

Identifiers

PMID32503307
PMCPMC7312011
OpenAlexW3033738814

What Socratic 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 Socratic graph.