In vitro bioeffects of the antiestrogen LY117018 on desmoid tumor and colon cancer cells

• Published in: Anticancer research Vol. 17; no. 3C; p. 2099
• Main Authors: Picariello, L, Fiorelli, G, Benvenuti, S, Brandi, M L, Galli, G, Malentacchi, C, Montali, E, Bigozzi, U, Ficari, F, Tonelli, F
• Format: Journal Article
• Language: English
• Published: Greece 01.05.1997
• Subjects: Adenocarcinoma; Binding Sites; Binding, Competitive; Cell Division - drug effects; Collagen - biosynthesis; Colonic Neoplasms; Colorectal Neoplasms; Dexamethasone - pharmacology; Estradiol - metabolism; Estrogen Antagonists - toxicity; Fibroblasts; Fibromatosis, Aggressive; Humans; Kinetics; Progesterone - pharmacology; Pyrrolidines - toxicity; Tamoxifen - pharmacology; Testosterone - pharmacology; Thiophenes - toxicity; Tumor Cells, Cultured
• ISSN: 0250-7005

Clinical and experimental evidence suggest that estrogen has a role in the natural history of desmoid tumor (DT) and colorectal carcinoma. The biological effects of LY117018, a nonsteroidal antiestrogen benzothiophene derivative, were assessed on a human adenocarcinoma cell line (HCT8 cells), and on DT cells and colorectal cancer derived fibroblasts in primary culture. LY117018 inhibited cell proliferation and collagen type I synthesis in DT cells. The compound also reduced cell growth in HCT8 cells and colorectal cancer fibroblasts. Binding experiments revealed the presence of estrogen binding sites in DT cells and frozen tissues but LY117018 did not displace [3H]17 beta E2 binding to DT cells. Present results demonstrate that LY117018 inhibits epithelial and fibroblastic colon cancer cells proliferation and proliferation and differentiation of desmoid cells in vitro. The lack of displacement of [3H]17 beta E2 binding to desmoid cells by LY117018 suggests the existence of distinct LY117018 binding sites.