title: Relationship of p21 (waf1/cip1) and differentiation in chondrosarcoma cells.
abstract: The histological grade of chondrosarcoma correlates well with their clinical behavior and with the patient's survival duration. We have previously demonstrated that p21 was expressed in the hypertrophic chondrocytes of the growth plate. To assess the relationship of p21 (waf1/cip1) to cell differentiation in chondrosarcoma, we examined the p21 expression in 14 cases of chondrosarcoma immunohistochemically and the induction of p21 by insulin-like growth factor-I (IGF-I) during cell differentiation in SW1353 chondrosarcoma cells. p21 immunoreactivity was seen in well-differentiated chondrosarcoma cells and was mutually exclusive with MIB1 reactivity in grade-1 chondrosarcoma. In vitro, the proteoglycan synthesis of SW1353 cells was increased by IGF-I in a dose-dependent manner. However, cell proliferation was not markedly stimulated. Overexpressions of p21 mRNA and p21 protein in SW1353 cells were induced by IGF-I 100 ng/ml. Our results suggested that the p21 expression was directly related to tumor differentiation and that the p21 expression was an important mediator for IGF-I in chondrosarcoma cells.
authors.affiliation: Department of Orthopedic Surgery, Kurume University School of Medicine, 67 Asahi-machi, Kurume, 830-0011, Japan. khiraoka@med.kurume-u.ac.jp
authors.forename: Koji
authors.initials: K
authors.lastname: Hiraoka
authors.forename: Michihisa
authors.initials: M
authors.lastname: Zenmyo
authors.forename: Setsuro
authors.initials: S
authors.lastname: Komiya
authors.forename: Rikimaru
authors.initials: R
authors.lastname: Kawabata
authors.forename: Masahiro
authors.initials: M
authors.lastname: Yokouchi
authors.forename: Ritsu
authors.initials: R
authors.lastname: Suzuki
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Hamada
authors.forename: Seiya
authors.initials: S
authors.lastname: Kato
authors.forename: Kensei
authors.initials: K
authors.lastname: Nagata
mesh_terms: D034961:Antigens, Nuclear; D001859:Bone Neoplasms / Q000737:chemistry / Q000378:metabolism* / Q000473:pathology; D002454:Cell Differentiation / Q000502:physiology*; D002455:Cell Division / Q000187:drug effects; D019902:Chondrocytes / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D002813:Chondrosarcoma / Q000737:chemistry / Q000378:metabolism* / Q000473:pathology; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000096:biosynthesis* / Q000235:genetics; D004305:Dose-Response Relationship, Drug; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology; D009687:Nuclear Proteins / Q000032:analysis; D011509:Proteoglycans / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D012334:RNA, Neoplasm / Q000032:analysis; D014407:Tumor Cells, Cultured / Q000187:drug effects
chemical_list: D034961:Antigens, Nuclear; C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D009687:Nuclear Proteins; D011509:Proteoglycans; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D007334:Insulin-Like Growth Factor I