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Peer-reviewedCC BYNutrients

Hexokinase II as a Potential Target of Apigenin Through the Induction of Apoptosis and Necroptosis in Malignant Mesothelioma

  • Moon-Kyun Cho1,2
  • Sang-Han Lee2,3
  • Hae-Seon Nam2,4
  • Yoon-Jin Lee2,3
4 affiliations
  1. 1Department of Dermatology, Soonchunhyang University Hospital, Seoul 04401, Republic of Korea
  2. 2Division of Molecular Cancer Research, Soonchunhyang Medical Research Institute, Soonchunhyang University, Cheonan 31511, Republic of Korea
  3. 3Department of Biochemistry, College of Medicine, Soonchunhyang University, Cheonan 31511, Republic of Korea
  4. 4Department of Tropical Medicine, College of Medicine, Soonchunhyang University, Cheonan 31511, Republic of Korea
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Abstract

Background: Lactate-acclimated MSTO-211HAcT and H2452AcT malignant mesothelioma (MM) cells were previously found to tolerate gemcitabine more readily than their parental cells while remaining sensitive to apigenin. We examined whether changes in glucose metabolism and HKII contribute to the apigenin response. Methods: Apigenin was evaluated in monolayer and spheroid cultures and in a xenograft model; HKII was also silenced in the acclimated cells. Results: Apigenin reduced cell viability, p-AKT (Ser473), glycolysis-associated proteins including HKII, and mitochondrial electron transport chain proteins, while increasing p53 and markers of cell death. Tumor growth and selected metabolic proteins were reduced in the xenograft model. HKII silencing reduced cell viability and glucose utilization, lowered cellular ATP, altered mitochondrial membrane potential, and increased markers of apoptosis and necroptosis. Conclusions: HKII-associated metabolism contributes to survival of lactate-acclimated MM cells, and apigenin affects this metabolic phenotype. Direct targeting of HKII by apigenin and the complete mitochondrial apoptotic pathway require further study.

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Cite

BibTeXRIS
BibTeX
@article{cho2026hexokinase,
  title = {{Hexokinase II as a Potential Target of Apigenin Through the Induction of Apoptosis and Necroptosis in Malignant Mesothelioma}},
  author = {Moon-Kyun Cho and Sang-Han Lee and Hae-Seon Nam and Yoon-Jin Lee},
  journal = {Nutrients},
  year = {2026},
  month = oct,
  doi = {10.3390/nu18193276},
  url = {https://europepmc.org/article/PMC/PMC13666630},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Hexokinase II as a Potential Target of Apigenin Through the Induction of Apoptosis and Necroptosis in Malignant Mesothelioma
AU  - Moon-Kyun Cho
AU  - Sang-Han Lee
AU  - Hae-Seon Nam
AU  - Yoon-Jin Lee
PY  - 2026
DA  - 2026/10/01
JO  - Nutrients
DO  - 10.3390/nu18193276
UR  - https://europepmc.org/article/PMC/PMC13666630
AB  - Background: Lactate-acclimated MSTO-211HAcT and H2452AcT malignant mesothelioma (MM) cells were previously found to tolerate gemcitabine more readily than their parental cells while remaining sensitive to apigenin. We examined whether changes in glucose metabolism and HKII contribute to the apigenin response. Methods: Apigenin was evaluated in monolayer and spheroid cultures and in a xenograft model; HKII was also silenced in the acclimated cells. Results: Apigenin reduced cell viability, p-AKT (Ser473), glycolysis-associated proteins including HKII, and mitochondrial electron transport chain proteins, while increasing p53 and markers of cell death. Tumor growth and selected metabolic proteins were reduced in the xenograft model. HKII silencing reduced cell viability and glucose utilization, lowered cellular ATP, altered mitochondrial membrane potential, and increased markers of apoptosis and necroptosis. Conclusions: HKII-associated metabolism contributes to survival of lactate-acclimated MM cells, and apigenin affects this metabolic phenotype. Direct targeting of HKII by apigenin and the complete mitochondrial apoptotic pathway require further study.
SN  - 2072-6643
ER  -