Tier 3 — preclinical

Betaine induces ferroptotic stress by enhancing KEAP1-mediated NRF2 degradation in breast cancer cells

Yingni Xu, Xiangmei Ye, Ji Lin, Xiaohui Guo, Zhengjin Liu
Cellular signalling 2026 146:112664

Bibliography

PubMed
PMID 42263898
Funding
Funding was not specified in the indexed record or accessible funding metadata.
Competing interests
Reported disclosure: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Study snapshot

DesignExperimental animal and/or laboratory research
ModelBreast-cancer cell lines and computational analyses
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionBetaine in MDA-MB-231 and MCF-7 cells
DurationIn vitro experimental protocols
EndpointsCancer-cell growth; Ferroptosis; KEAP1/NRF2

What the study showed, in plain terms

Published in 2026, this source examined preclinical aging, brain and metabolic mechanisms. Design: Experimental animal and/or laboratory research. Sample/model: Experiment-specific biological replicates and model groups; see original methods. The exposure or intervention was Betaine in MDA-MB-231 and MCF-7 cells. Follow-up or treatment period: In vitro experimental protocols.

Betaine increased ferroptosis-associated stress and reduced selected malignant cell behaviors, involving KEAP1/NRF2 regulation.

Experimental model evidence. The intervention, concentrations and outcomes do not establish an effective human supplement dose or a clinical treatment benefit.

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Key findings

  • Betaine increased ferroptosis-associated stress and reduced selected malignant cell behaviors, involving KEAP1/NRF2 regulation.
  • The recorded outcome domains were Cancer-cell growth; Ferroptosis; KEAP1/NRF2.
  • The result applies to the tested exposure: Betaine in MDA-MB-231 and MCF-7 cells; In vitro experimental protocols.

What this study can and cannot tell us

  • Experimental model evidence. The intervention, concentrations and outcomes do not establish an effective human supplement dose or a clinical treatment benefit.
  • Cell concentrations, species, disease models and experimental routes cannot be converted directly into an effective or safe oral human regimen.
  • Source basis: Indexed abstract and bibliographic data. Missing method details, funding information or participant denominators are not inferred.

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