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The HPV-16 E5 oncogene and bafilomycin A(1) influence cell motility
P Thomsen1, O Rudenko, V Berezin
1The Protein Laboratory, Institute of Molecular Pathology, University of Copenhagen, Panum Institute, Bldg. 6.2, Blegdamsvej 3C, DK-2200, Copenhagen N, Denmark.
Biochimica Et Biophysica Acta
|December 11, 1999
Summary
The vacuolar H(+)-ATPase is crucial for normal cell motility. Its inhibition by bafilomycin A(1) or the HPV-16 E5 oncogene impairs cell movement and alters morphology.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- The vacuolar H(+)-ATPase (V-ATPase) is essential for maintaining pH gradients in intracellular compartments.
- Inhibition of V-ATPase function can disrupt cellular processes, including endocytosis.
- The HPV-16 E5 oncoprotein is known to interact with the V-ATPase.
Purpose of the Study:
- To investigate the impact of V-ATPase inhibition on NIH3T3 cell morphology and motility.
- To determine the effect of the HPV-16 E5 oncoprotein on cell motility.
- To explore the combined effects of V-ATPase inhibition and E5 expression on cell locomotion.
Main Methods:
- Utilizing bafilomycin A(1) to inhibit V-ATPase activity.
- Transfecting NIH3T3 cells with the HPV-16 E5 oncogene.
- Employing computer-assisted video recordings and image analysis to assess cell morphology and motility.
Main Results:
- Inhibition of V-ATPase by bafilomycin A(1) or E5 expression significantly reduced NIH3T3 cell motility.
- Both treatments led to observable changes in cell morphology.
- Bafilomycin A(1) potentiated the effect of the E5 protein on cell motility, suggesting cooperative or additive mechanisms.
Conclusions:
- Proper function of the vacuolar H(+)-ATPase is indispensable for normal cell locomotion.
- The HPV-16 E5 oncoprotein affects cell motility, potentially through V-ATPase interaction or other targets.
- Combined inhibition of V-ATPase and E5 expression highlights the critical role of V-ATPase in cellular movement.