title: [In vitro study on the effect of sex steroid and growth factor on growth and laminin, collagen IV, and tissue plasminogen activator production of normal endometrial cells and endometrial cancer cells in culture].
abstract: The mechanism of the invasion and proliferation of endometrial cancer is closely related to interactions between the endometrial glands and stroma. In this study, we examined the biological role of sex steroids (estradiol; E2, progesterone; P) and growth factors (epidermal growth factor; EGF, transforming growth factor-beta; TGF-beta) on cell growth and laminin, collagen IV and tissue plasminogen activator (t-PA) production of normal endometrial cells and endometrial cancer cells in culture. Normal endometrial gland cells and stromal cells, and endometrial cancer cell lines (Ishikawa, OMC-2) were used. E2, P, EGF and TGF-beta were added to the culture in physiological concentrations. The growth of normal endometrial gland cells was promoted by E2 and EGF, whereas that of Ishikawa cells and OMC-2 cells was promoted by EGF. E2 enhanced the effects of EGF in normal endometrial gland cells. The growth of normal endometrial stromal cells was not affected by them. OMC-2 was inhibited by anti-EGF receptor antibody. On the other hand, the production of laminin and collagen IV of these cultured cells was inhibited by EGF and promoted by TGF-beta, whereas that of t-PA was promoted by EGF and inhibited by TGF-beta. These results suggest that the growth of normal endometrial gland cells with estrogen receptor (ER) is controlled by both E2 and EGF, whereas that of endometrial cancer cells is affected only by EGF, and those cells without ER depend particularly on the autocrine growth mechanism of EGF.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Obstetrics and Gynecology, Osaka Medical College.
authors.forename: M
authors.initials: M
authors.lastname: Ueda
authors.forename: M
authors.initials: M
authors.lastname: Ueki
authors.forename: T
authors.initials: T
authors.lastname: Tsurunaga
authors.forename: T
authors.initials: T
authors.lastname: Yamada
authors.forename: Y
authors.initials: Y
authors.lastname: Okamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Seiki
authors.forename: E
authors.initials: E
authors.lastname: Iwai
authors.forename: O
authors.initials: O
authors.lastname: Sugimoto
mesh_terms: D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D003094:Collagen / Q000096:biosynthesis*; D016889:Endometrial Neoplasms / Q000378:metabolism / Q000473:pathology*; D004717:Endometrium / Q000166:cytology* / Q000378:metabolism; D004815:Epidermal Growth Factor / Q000494:pharmacology* / Q000502:physiology; D004958:Estradiol / Q000494:pharmacology* / Q000502:physiology; D005260:Female; D006801:Humans; D007797:Laminin / Q000096:biosynthesis*; D011374:Progesterone / Q000494:pharmacology / Q000502:physiology; D010959:Tissue Plasminogen Activator / Q000096:biosynthesis*; D016212:Transforming Growth Factor beta / Q000494:pharmacology / Q000502:physiology; D014407:Tumor Cells, Cultured
chemical_list: D007797:Laminin; D016212:Transforming Growth Factor beta; D011374:Progesterone; D004958:Estradiol; D004815:Epidermal Growth Factor; D003094:Collagen; D010959:Tissue Plasminogen Activator