Evidence map›Paper›PMID 32266287›Full record

ReviewFrontiers in molecular biosciences2020

ZEB1: A Critical Regulator of Cell Plasticity, DNA Damage Response, and Therapy Resistance.

Stanislav Drápela, Jan Bouchal, Mohit Kumar Jolly, Zoran Culig, Karel Souček

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in molecular biosciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
9.8field-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

96 citing papers in PubMed, 170 citations in OpenAlex.

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  12. CD44 and Snail1 Expression Predicts Poor Prognosis of Oral Squamous Cell Carcinoma.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2025
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36 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

5 authors at 5 institutions in 3 countries.

Stanislav DrápelaDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, Brno, Czechia.
Jan BouchalDepartment of Clinical and Molecular Pathology, Faculty of Medicine and Dentistry, Institute of Molecular and Translational Medicine, Palacky University, Olomouc, Czechia.
Mohit Kumar JollyCentre for BioSystems Science and Engineering, Indian Institute of Science, Bangalore, India.
Zoran CuligInternational Clinical Research Center, Center for Biomolecular and Cellular Engineering, St. Anne's University Hospital in Brno, Brno, Czechia.
Karel SoučekDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, Brno, Czechia.
Czech Academy of Sciences, Institute of Biophysics · CZIndian Institute of Science Bangalore · INMasaryk University · CZPalacký University Olomouc · CZSt. Anne's University Hospital Brno · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The predominant way in which conventional chemotherapy kills rapidly proliferating cancer cells is the induction of DNA damage. However, chemoresistance remains the main obstacle to therapy effectivity. An increasing number of studies suggest that epithelial-to-mesenchymal transition (EMT) represents a critical process affecting the sensitivity of cancer cells to chemotherapy. Zinc finger E-box binding homeobox 1 (ZEB1) is a prime element of a network of transcription factors controlling EMT and has been identified as an important molecule in the regulation of DNA damage, cancer cell differentiation, and metastasis. Recent studies have considered upregulation of ZEB1 as a potential modulator of chemoresistance. It has been hypothesized that cancer cells undergoing EMT acquire unique properties that resemble those of cancer stem cells (CSCs). These stem-like cells manifest enhanced DNA damage response (DDR) and DNA repair capacity, self-renewal, or chemoresistance. In contrast, functional experiments have shown that ZEB1 induces chemoresistance regardless of whether other EMT-related changes occur. ZEB1 has also been identified as an important regulator of DDR by the formation of a ZEB1/p300/PCAF complex and direct interaction with ATM kinase, which has been linked to radioresistance. Moreover, ATM can directly phosphorylate ZEB1 and enhance its stability. Downregulation of ZEB1 has also been shown to reduce the abundance of CHK1, an effector kinase of DDR activated by ATR, and to induce its ubiquitin-dependent degradation. In this perspective, we focus on the role of ZEB1 in the regulation of DDR and describe the mechanisms of ZEB1-dependent chemoresistance.

Indexed as

DNA damage responseEMT-epithelial to mesenchymal transitionplasticitytherapy resistanceZEB1

Identifiers

PMID32266287
PMCPMC7096573
OpenAlexW3011792328

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.