Microvesicles released from tumor cells disrupt epithelial cell morphology and contractility
Francois Bordeleau1, Bryan Chan1, Marc A Antonyak2
1Department of Biomedical Engineering, Cornell University, Ithaca, NY 14853, United States.
Cancer cell-derived microvesicles (MVs) prompt non-malignant epithelial cells to reorganize the extracellular matrix (ECM). This process involves increased cell contractility and is crucial for tumor microenvironment remodeling.
Area of Science:
- Cell Biology
- Cancer Research
- Biophysics
Background:
- Tumor progression involves complex interactions between cancer cells and their microenvironment.
- Cancer cell-derived microvesicles (MVs) mediate intercellular communication.
- Extracellular matrix (ECM) remodeling is a hallmark of cancer progression, typically attributed to fibroblasts.
Purpose of the Study:
- To investigate the role of cancer cell-derived MVs in influencing non-malignant epithelial cells.
- To determine if non-malignant epithelial cells can participate in ECM reorganization upon MV treatment.
- To elucidate the cellular mechanisms underlying MV-induced ECM changes.
Main Methods:
- Utilized MCF10a (non-malignant breast epithelial) cells and MVs from MDA-MB-231 (aggressive breast carcinoma) cells.
- Cultured cells in 3D collagen matrices to observe ECM reorganization.
- Measured cellular traction force, acto-myosin contractility, and focal adhesion kinase (FAK) activity.
Main Results:
- Non-malignant epithelial cells, treated with cancer cell-derived MVs, actively reorganized 3D collagen matrices.
- MV treatment induced significant changes in epithelial cell behavior under 3D culture.
- Observed increased cellular traction force, acto-myosin contractility, and FAK activity post-MV treatment.
Conclusions:
- Cancer cell-derived MVs can induce non-malignant epithelial cells to remodel the ECM.
- Enhanced epithelial cell contractility, driven by MVs, contributes to ECM reorganization.
- This highlights a novel mechanism by which tumor cells influence their microenvironment, potentially impacting metastasis.
More Related Videos
10:55Analyzing the Communication Between Monocytes and Primary Breast Cancer Cells in an Extracellular Matrix Extract ECME-based Three-dimensional System
Published on: January 8, 2018
13:34High Throughput Traction Force Microscopy Using PDMS Reveals Dose-Dependent Effects of Transforming Growth Factor-β on the Epithelial-to-Mesenchymal Transition
Published on: June 1, 2019
Related Concept Videos
The Tumor Microenvironment
The Tumor Microenvironment
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Cancer Cell Migration through Invadopodia
Cell Motility through Blebbing
Blebbing Through the Matrix
In multicellular...
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
