Xp95, a protein recently identified in Xenopus laevis, is potentially invol
ved in progesterone-induced Xenopus oocyte maturation. In this study, we cl
oned a human homologue of Xp95, designated Hp95, and examined the effect of
its overexpression on the growth properties of human malignant HeLa cells
which have lost the contact inhibition of cell proliferation. We observed t
hat although HeLa cells did not undergo GI phase arrest at any stage after
confluence, they were able to downregulate their GI phase CDK activities in
response to confluence. When Hp95 was overexpressed in HeLa cells by trans
fection with a constitutive or an inducible expression vector containing a
full-length Hp95 transgene, HeLa cells became able to undergo Gl phase arre
st and form a monolayer culture after confluence. However, the GI phase CDK
activities in these Hp95 overexpressing cells were not inhibited further a
s compared to control cells after confluence. These results indicate that t
he defects in HeLa cells that cause the loss of contact inhibition of cell
proliferation are in components downstream of the GI phase CDKs and that ov
erexpression of Hp95 counteracts some of these defects.