Endometrial carcinoma cells are nonpermissive for CD44-erbB2 interactions.
The erbB2 receptor tyrosine kinase and the CD44 transmembrane glycoprotein interact with one another in numerous cell types. This interaction helps to maintain erbB2 activity that contributes to tumor progression. We investigated whether CD44 and erbB2 similarly interact in endometrial carcinomas in vitro and in situ. In contrast to other carcinomas, CD44 did not colocalize with erbB2 in any of the 51 cases of endometrial cancer analyzed. CD44 also did not coimmunoprecipitate or colocalize with erbB2 in two endometrial carcinoma cell lines. We propose that the lack of CD44-erbB2 interactions may reduce the contribution of erbB2 to endometrial carcinoma progression.
Wobus
Manja
M
Department of Cell Biology, Neurobiology and Anatomy, Vontz Center for Molecular Studies, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0521, USA.
Kuns
Robin
R
Sheyn
Irene
I
Werness
Bruce A
BA
Husseinzadeh
Nader
N
Aron
Bernard S
BS
Sherman
Larry S
LS
D016889:Endometrial Neoplasms / Q000378:metabolism*; D005260:Female; D006801:Humans; D018960:Hyaluronan Receptors / Q000378:metabolism*; D007150:Immunohistochemistry; D011379:Prognosis; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism*; D014407:Tumor Cells, Cultured
D018960:Hyaluronan Receptors; D018719:Erb-b2 Receptor Tyrosine Kinases