Resistance to the growth inhibitory effects of transforming growth factor-beta (TGF-beta) is a characteristic of many transformed cells. The purpose of this study was to determine the response of ovarian cancer cells to TGF-beta1 and to investigate the roles of components of the TGF-beta/Smads signaling pathway in carcinogenesis of ovarian cancer. Three ovarian cancer cell lines, HO-8910, HO-8910PM and SKOV3, were treated with TGF-beta1 and assayed for growth response by MTT assay. Furthermore, expression and subcellular localization of the components of TGF-beta/Smads signaling pathway in these cell lines in the absence or presence of TGF-beta1 were determined by RT-PCR and immunofluorescence analysis. We found that proliferation of SKOV3 cell was not significantly inhibited by TGF-beta1 while it expressed all components of the TGF-beta/Smads signaling pathway. After exposure to TGF-beta1, Smad7 protein in SKOV3 increased transiently and translocated to cytoplasm from nucleus while P-Smad2 translocated into nucleus from cytoplasm. Taken together, the results suggested that the TGF-beta/Smads signaling pathway remained functional in human ovarian cancer cells, HO-8910, HO-8910PM and SKOV3, and the abnormalities of the downstream effectors of Smads proteins might contribute to the resistance of SKOV3 cell to TGF-beta1.