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Updated: May 1, 2026

Assessment of Mitochondrial Health in Cancer-Associated Fibroblasts Isolated from 3D Multicellular Lung Tumor Spheroids
Published on: October 21, 2022
Lung cancer-associated myofibroblasts reveal distinctive ultrastructure and function
Henna M Karvonen1, Siri T Lehtonen, Raija T Sormunen
1*Department of Internal Medicine/Respiratory Research Unit, Institute of Clinical Medicine, University of Oulu, Oulu, Finland; †Department of Medicine, Respiratory Research Unit and Medical Research Center Oulu, Oulu University Hospital, Oulu, Finland; ‡Department of Anatomy and Cell Biology, Institute of Biomedicine, §Biocenter Oulu, and ‖Department of Pathology, Institute of Diagnostics, University of Oulu, Oulu, Finland; ¶Department of Pathology, Oulu University Hospital, Oulu, Finland; #Department of Medicine, Division of Respiratory Medicine, Karolinska Institutet, Karolinska University Hospital Solna, Stockholm, Sweden; **Unit of Medicine and Clinical Research, Pulmonary Division, University of Eastern Finland, Kuopio, Finland; and ††Center for Medicine and Clinical Research, Division of Respiratory Medicine, Kuopio University Hospital, Kuopio, Finland.
Lung cancer stromal cells show distinct ultrastructure and function compared to normal lung cells. Smoking impacts myofibroblast characteristics, influencing cancer progression.
Area of Science:
- Oncology
- Cell Biology
- Biochemistry
Background:
- Cancer-associated stromal cells influence tumor growth through interactions with carcinoma cells.
- Stromal cells play a critical role in the tumor microenvironment.
Purpose of the Study:
- To characterize the ultrastructure and contractile properties of stromal cells from lung cancer.
- To compare these properties with stromal cells from tumor-free lung tissue.
Main Methods:
- Transmission electron microscopy and 3D collagen gel contraction assays were used.
- Expression of alpha-smooth muscle actin (α-SMA) was analyzed via immunoelectron microscopy and Western blotting.
Main Results:
- Lung cancer stromal cells exhibited more myofibroblastic features and higher α-SMA expression than normal lung cells.
- Cancer-associated fibroblasts showed greater contractile capacity in collagen gels.
- Smoking altered myofibroblastic phenotype, reducing α-SMA in smokers' lung cancer cells.
Conclusions:
- Lung cancer-associated myofibroblasts differ ultrastructurally and functionally from those in tumor-free lung.
- Smoking significantly alters the myofibroblastic phenotype, irrespective of cell origin.
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