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Sorafenib and nitazoxanide disrupt mitochondrial function and inhibit regrowth capacity in three-dimensional models of hepatocellular and colorectal carcinoma
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cancer Pharmacology and Computational Medicine.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cancer Pharmacology and Computational Medicine.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cancer Pharmacology and Computational Medicine.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cancer Pharmacology and Computational Medicine.
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2022 (English)In: Scientific Reports, E-ISSN 2045-2322, Vol. 12, article id 8943Article in journal (Refereed) Published
Abstract [en]

Quiescent cancer cells in malignant tumors can withstand cell-cycle active treatment and cause cancer spread and recurrence. Three-dimensional (3D) cancer cell models have led to the identification of oxidative phosphorylation (OXPHOS) as a context-dependent vulnerability. The limited treatment options for advanced hepatocellular carcinoma (HCC) and colorectal carcinoma (CRC) metastatic to the liver include the multikinase inhibitors sorafenib and regorafenib. Off-target effects of sorafenib and regorafenib are related to OXPHOS inhibition; however the importance of this feature to the effect on tumor cells has not been investigated in 3D models. We began by assessing global transcriptional responses in monolayer cell cultures, then moved on to multicellular tumor spheroids (MCTS) and tumoroids generated from a CRC patient. Cells were treated with chemotherapeutics, kinase inhibitors, and the OXPHOS inhibitors. Cells grown in 3D cultures were sensitive to the OXPHOS inhibitor nitazoxanide, sorafenib, and regorafenib and resistant to other multikinase inhibitors and chemotherapeutic drugs. Furthermore, nitazoxanide and sorafenib reduced viability, regrowth potential and inhibited mitochondrial membrane potential in an additive manner at clinically relevant concentrations. This study demonstrates that the OXPHOS inhibition caused by sorafenib and regorafenib parallels 3D activity and can be further investigated for new combination strategies.

Place, publisher, year, edition, pages
Springer Nature Springer Nature, 2022. Vol. 12, article id 8943
National Category
Cancer and Oncology
Identifiers
URN: urn:nbn:se:uu:diva-476608DOI: 10.1038/s41598-022-12519-4ISI: 000800769400038PubMedID: 35624293OAI: oai:DiVA.org:uu-476608DiVA, id: diva2:1676585
Funder
Swedish Cancer SocietyAvailable from: 2022-06-27 Created: 2022-06-27 Last updated: 2024-01-15Bibliographically approved
In thesis
1. Quiescent cancer cells: Three-dimensional cell models for evaluation of new therapeutics
Open this publication in new window or tab >>Quiescent cancer cells: Three-dimensional cell models for evaluation of new therapeutics
2022 (English)Licentiate thesis, comprehensive summary (Other academic)
Alternative title[sv]
Vilande cancerceller : Tredimensionella cellmodeller för utvärdering av nya cancerläkemedel
Abstract [en]

Inadequate metabolic conditions in solid tumors lead to the formation of quiescent cancer cells that are suspended in a transient cell cycle arrest. When conditions change, quiescent cancer cells can re-enter the cell cycle and cause recurrence. Drug screening efforts have revealed mitochondrial oxidative phosphorylation as a unique metabolic dependency in quiescent cancer cells. The anthelmintic drug nitazoxanide is an inhibitor of oxidative phosphorylation and preferentially active against quiescent cancer cells in multicellular tumor spheroids. 

In this thesis, we employed current and developed new models of quiescent cancer cells and applied live cell imaging for improved preclinical evaluation of cancer drugs in hepatocellular and colorectal carcinoma cell lines. As part of this work, a new assay to measure mitochondrial membrane potential in three-dimensional cell models was developed, an application of the JC-1 assay, and we demonstrated that the preferential activity against quiescent cancer cells of nitazoxanide is shared by two kinase inhibitors: sorafenib and regorafenib. The sensitivity of quiescent cancer cells to nitazoxanide, sorafenib, and regorafenib correlated with the disruption of the mitochondrial membrane potential. Nitazoxanide and sorafenib, in combination, caused an additive decrease in viability, mitochondrial membrane potential, and colony regrowth capacity. 

Furthermore, we developed a quiescent hollow fiber assay and implemented an improved analysis using live cell imaging and adenosine triphosphate analysis. Hypoxia and cancer cell quiescence were enriched in hollow fiber macrocapsules over time, and the culture conditions affected nitazoxanide sensitivity. Additionally, we used basement membrane extract gel to support cell growth in hollow fiber macrocapsules and implanted macrocapsules in mice. We observed that the in vivo environment was favorable to cell growth. Through this characterization of the quiescent hollow fiber assay, we were able to outline important paths for future research. 

Place, publisher, year, edition, pages
Uppsala: Uppsala universitet, 2022. p. 58
Keywords
Cancer, cancer cell quiescence, dormancy, three-dimensional, multicellular tumor spheroids, model development, cancer pharmacology, mitochondria, OXPHOS, colorectal carcinoma, hepatocellular carcinoma
National Category
Cancer and Oncology
Research subject
Medical Science
Identifiers
urn:nbn:se:uu:diva-483620 (URN)
Presentation
2022-10-05, Hedstrandsalen, Akademiska sjukhuset ingång 70, Uppsala, 09:00 (English)
Supervisors
Available from: 2022-09-14 Created: 2022-09-09 Last updated: 2022-09-14Bibliographically approved

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Nyberg, FridaBlom, KristinSelvin, ToveRudfeldt, JakobAndersson, ClaesSenkowski, WojciechNygren, PeterLarsson, RolfJarvius, MalinFryknäs, Mårten

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Nyberg, FridaBlom, KristinSelvin, ToveRudfeldt, JakobAndersson, ClaesSenkowski, WojciechNygren, PeterLarsson, RolfJarvius, MalinFryknäs, Mårten
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Cancer Pharmacology and Computational MedicineExperimental and Clinical OncologyScience for Life Laboratory, SciLifeLabDepartment of Pharmaceutical Biosciences
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