Cited by 22Bacterial Genetics and BiotechnologyGene Regulatory Network AnalysisEvolution and Genetic Dynamics

Drug tolerance and persistence in bacteria, fungi and cancer cells: Role of non-genetic heterogeneity

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El Meouche, Imane, Jain, Paras, Jolly, Mohit Kumar, Capp, Jean-Pascal·2024·Translational Oncology

Abstract

A common feature of bacterial, fungal and cancer cell populations upon treatment is the presence of tolerant and persistent cells able to survive, and sometimes grow, even in the presence of usually inhibitory or lethal drug concentrations, driven by non-genetic differences among individual cells in a population. Here we review and compare data obtained on drug survival in bacteria, fungi and cancer cells to unravel common characteristics and cellular pathways, and to point their singularities. This comparative work also allows to cross-fertilize ideas across fields. We particularly focus on the role of gene expression variability in the emergence of cell-cell non-genetic heterogeneity because it represents a possible common basic molecular process at the origin of most persistence phenomena and could be monitored and tuned to help improve therapeutic interventions.

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Crossref · 10.1016/j.tranon.2024.102069

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  • Persister cells might obtain stronger antioxidant capacity by upregulating enzymes like SODs or alkyl hydroperoxide reductase 1.

    “As antifungals can increase levels of ROS, persister cells might obtain stronger antioxidant capacity by upregulating enzymes, like superoxide dismutases (SODs) or alkyl hydroperoxide reductase 1, etc. [127].”

    From Insight into the Mechanisms and Clinical Relevance of Antifungal Heteroresistance (2025) · cites this paper as [127]

    The Fungal persisters section says antifungals produce ROS and that C. albicans persisters highly express SODs, which protect against miconazole-induced ROS. It says AHP1 correlates with persister levels in biofilms, but does not say persisters upregulate AHP1 or establish that it increases their antioxidant capacity. No page number is available in our copy. (LLM, conf=0.85)

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Research works printed but not linked: 2

  1. [24]Andersson D.I. Nicoloff H. Hjort K. Mechanisms and clinical relevance of bacterial heteroresistance Nat. Rev. Microbiol. 17 2019 479 496 31235888
  2. [38]El Meouche I. Siu Y. Dunlop M.J. Stochastic expression of a multiple antibiotic resistance activator confers transient resistance in single cells Sci. Rep. 6 2016 19538 26758525 PMC4725842

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Authors
El Meouche, I., Jain, P., Jolly, M. K., & Capp, J.-P.
Affiliations
  • Indian Institute of Science Bangalore (IN)
  • Centre National de la Recherche Scientifique (FR)
Corresponding author
Capp, Jean-Pascal
Venue
Translational Oncology
Publisher
Elsevier BV
Published
2024-11
Volume
49
Pages
102069
ISSN
1936-5233 (ISSN-L)
OpenAlex
W4401412353
Cited by
22
References
144
Citations by year
2026: 11 · 2025: 10 · 2024: 1
FWCI
5.84
Type
journal article
Language
en
Open access
Locations
  • Translational Oncology (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • NOT FOUND REPOSITORY (Indian Institute of Science Bangalore) (acceptedVersion)
  • HAL (submittedVersion, cc-by-nc-nd)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gene Regulatory Network Analysis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Evolution and Genetic Dynamics
Keywords
drug tolerance, bacterial persistence, fungal persistence, cancer cell persistence, non-genetic heterogeneity, gene expression variation, antibiotic resistance, antifungal resistance, cancer chemotherapy resistance

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