Related Experiment Videos
Modulation of tumor cell motility by plasmin
L Chikahisa1, K Matsuo, Y Yamada
1Cancer Research Laboratory, Hanno Research Center, Taiho Pharmaceutical Co., Hanno, Saitama, Japan.
Invasion & Metastasis
|January 1, 1997
Summary
Plasmin enhances tumor cell movement, particularly with laminin, through a chemokinetic effect. This process is blocked by alpha2-antiplasmin and involves protein kinase C and mitogen-activated protein kinase pathways.
Area of Science:
- Biochemistry
- Cell Biology
- Oncology
Background:
- Tumor cell motility is crucial for metastasis.
- Extracellular matrix proteins influence cell behavior.
- Plasmin's role in cell migration requires further elucidation.
Purpose of the Study:
- To investigate the effect of plasmin on tumor cell motility.
- To identify specific extracellular matrix proteins involved in plasmin-mediated motility.
- To explore the signaling pathways modulated by plasmin and extracellular matrix interactions.
Main Methods:
- Utilized a pure chemotactic model.
- Assessed motility of human melanoma LOX and lung cancer Lu-99 cells.
- Tested the effects of various extracellular matrix proteins, alpha2-antiplasmin, and signal transduction kinase inhibitors.
Main Results:
- Plasmin facilitated tumor cell motility in the presence of extracellular matrix proteins, with laminin showing the most significant contribution.
- The induced cell motility was chemokinetic and was largely inhibited by alpha2-antiplasmin.
- Signal transduction inhibitors indicated that plasmin modulates cell motility via protein kinase C and mitogen-activated protein kinase cascades, in conjunction with laminin.
Conclusions:
- Plasmin, especially in cooperation with laminin, significantly enhances tumor cell motility through a chemokinetic mechanism.
- The plasmin-induced motility is mediated by protein kinase C and mitogen-activated protein kinase signaling pathways.
- Alpha2-antiplasmin effectively suppresses plasmin-driven tumor cell migration.