Assessing the metastatic potential of circulating tumor cells using an organ-on-chip model.

Autor:	Schmid KF; Organs-on-chip Technologies Laboratory, ARTORG Center, University of Bern, Bern, Switzerland.; Graduate School of Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland., Zeinali S; Organs-on-chip Technologies Laboratory, ARTORG Center, University of Bern, Bern, Switzerland., Moser SK; Organs-on-chip Technologies Laboratory, ARTORG Center, University of Bern, Bern, Switzerland., Dubey C; Department of General Thoracic Surgery, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland., Schneider S; Organs-on-chip Technologies Laboratory, ARTORG Center, University of Bern, Bern, Switzerland., Deng H; Department of General Thoracic Surgery, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.; Department of BioMedical Research, University of Bern, Bern, Switzerland., Haefliger S; Department of Medical Oncology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland., Marti TM; Department of General Thoracic Surgery, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.; Department of BioMedical Research, University of Bern, Bern, Switzerland., Guenat OT; Organs-on-chip Technologies Laboratory, ARTORG Center, University of Bern, Bern, Switzerland.; Department of General Thoracic Surgery, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.; Department of Pulmonary Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
Jazyk:	angličtina
Zdroj:	Frontiers in bioengineering and biotechnology [Front Bioeng Biotechnol] 2024 Oct 08; Vol. 12, pp. 1457884. Date of Electronic Publication: 2024 Oct 08 (Print Publication: 2024).
DOI:	10.3389/fbioe.2024.1457884
Abstrakt:	Metastatic lung cancer remains a leading cause of death worldwide, with its intricate metastatic cascade posing significant challenges to researchers and clinicians. Despite substantial progress in understanding this cascade, many aspects remain elusive. Microfluidic-based vasculature-on-chip models have emerged as powerful tools in cancer research, enabling the simulation of specific stages of tumor progression. In this study, we investigate the extravasation behaviors of A549 lung cancer cell subpopulations, revealing distinct differences based on their phenotypes. Our results show that holoclones, which exhibit an epithelial phenotype, do not undergo extravasation. In contrast, paraclones, characterized by a mesenchymal phenotype, demonstrate a notable capacity for extravasation. Furthermore, we observed that paraclones migrate significantly faster than holoclones within the microfluidic model. Importantly, we found that the depletion of vascular endothelial growth factor (VEGF) effectively inhibits the extravasation of paraclones. These findings highlight the utility of microfluidic-based models in replicating key aspects of the metastatic cascade. The insights gained from this study underscore the potential of these models to advance precision medicine by facilitating the assessment of patient-specific cancer cell dynamics and drug responses. This approach could lead to improved strategies for predicting metastatic risk and tailoring personalized cancer therapies, potentially involving the sampling of cancer cells from patients during tumor resection or biopsies. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2024 Schmid, Zeinali, Moser, Dubey, Schneider, Deng, Haefliger, Marti and Guenat.)
Databáze:	MEDLINE
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