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Cellular Mg2+ decrease causes a distinctive NF-κB-dependent form of cell death.

Koyuki Kawamura1, Koya Ono2, Eikan Mishima3

  • 1Laboratory of Biorecognition Chemistry, Department of Synthetic Chemistry and Biological Chemistry, Graduate School of Engineering, Kyoto University, Katsura, Nishikyo-ku, Kyoto 615-8510, Japan.

Cell Reports
|February 11, 2026
PubMed
Summary
This summary is machine-generated.

Magnesium (Mg2+) is vital for cell function. Researchers found that reduced Mg2+ triggers a novel NF-κB-dependent cell death pathway, offering new insights into cellular regulation and cancer biology.

Keywords:
CNNMCP: cell biologyNF-κBPRLactin polymerizationmagnesiumregulated cell death

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Area of Science:

  • Cellular Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Magnesium ions (Mg2+) are crucial cofactors for numerous enzymes, playing a fundamental role in cellular processes.
  • The phosphatase of regenerating liver (PRL) protein family is often upregulated in cancer and inhibits cyclin M (CNNM) Mg2+ efflux transporters.

Purpose of the Study:

  • To investigate the physiological role of PRL in cellular Mg2+ homeostasis.
  • To elucidate the mechanisms underlying Mg2+ dysregulation-induced cell death.

Main Methods:

  • Utilized combined genetic knockout and knockdown approaches to study PRL.
  • Performed transcriptomic analysis to identify activated cellular pathways.
  • Investigated the role of the NF-κB pathway in Mg2+ homeostasis and cell death.
  • Examined the effects of CNNM overexpression on intracellular Mg2+ levels and cell viability.

Main Results:

  • PRL deletion significantly reduced intracellular Mg2+ levels, leading to extensive cell death.
  • Transcriptomic analysis revealed activation of the NF-κB pathway upon PRL deletion.
  • Genetic deletion of the NF-κB p65 subunit abrogated PRL deletion-induced cell death.
  • CNNM overexpression mimicked the effects of PRL deletion, causing Mg2+ decrease, NF-κB activation, and cell death.
  • Observed unique morphological features, including actin-driven protrusions, in this distinct cell death modality.

Conclusions:

  • Intracellular Mg2+ depletion triggers a novel mode of NF-κB-dependent cell death.
  • PRL and CNNM play critical roles in maintaining cellular Mg2+ homeostasis.
  • This Mg2+-dependent cell death pathway presents a new area for research in cellular regulation and cancer therapy.