[HTML][HTML] The HPV-16 E5 oncogene and bafilomycin A1 influence cell motility

P Thomsen, O Rudenko, V Berezin, B Norrild - Biochimica et Biophysica …, 1999 - Elsevier
P Thomsen, O Rudenko, V Berezin, B Norrild
Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, 1999Elsevier
It is known that the proper function of the vacuolar H+-ATPase is inhibited by bafilomycin A1.
In transfected cells the E5 protein interacts with the 16 kDa subunit of the vacuolar H+-
ATPase. Thereby the pH gradient in endocytic structures is impaired. The present study
demonstrates for the first time that the inhibition of the vacuolar H+-ATPase in NIH3T3 cells
with bafilomycin A1 or by transfection of cells with the HPV-16 E5 oncogene leads to a
changed morphology and a reduced motility as shown by computer-assisted video …
It is known that the proper function of the vacuolar H+-ATPase is inhibited by bafilomycin A1. In transfected cells the E5 protein interacts with the 16 kDa subunit of the vacuolar H+-ATPase. Thereby the pH gradient in endocytic structures is impaired. The present study demonstrates for the first time that the inhibition of the vacuolar H+-ATPase in NIH3T3 cells with bafilomycin A1 or by transfection of cells with the HPV-16 E5 oncogene leads to a changed morphology and a reduced motility as shown by computer-assisted video recordings and image analysis. Bafilomycin A1 potentiates the effect of the E5 protein on cell motility and this cooperative effect indicates that the E5 protein and bafilomycin A1 either target the vacuolar H+-ATPase differently or that the E5 protein has additional targets in transfected cells. Our data therefore show that proper function of the vacuolar H+-ATPase is needed for normal cell locomotion.
Elsevier