title: Fas-resistance in ATL cell lines not associated with HTLV-I or FAP-1 production.
abstract: A preventive role for human T-cell leukemia virus type-I (HTLV-I) and Fas-associated phosphatase-1 (FAP-1) in Fas-mediated apoptosis has been reported in HTLV-I-infected cells. In the present study, we examined whether these molecules increased during the acquisition of Fas-resistance in adult T-cell leukemia (ATL) cell lines. SO4, ST1 and KK1 are Fas-sensitive ATL cell lines, and produce small amounts of HTLV-I in vitro. Although their subclones RSO4 and RST1 are completely Fas-resistant, they produced an equivalent amount of HTLV-I to SO4 and ST1. Moreover, FAP-1 mRNA was not detected in these cell lines irrespective of Fas sensitivity. Thus, Fas resistance in ATL cells was not directly associated with the increased production of HTLV-I or FAP-1.
authors.affiliation: Department of Laboratory Medicine, Nagasaki University School of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Yamada
authors.forename: K
authors.initials: K
authors.lastname: Sugahara
authors.forename: K
authors.initials: K
authors.lastname: Tsuruda
authors.forename: K
authors.initials: K
authors.lastname: Nohda
authors.forename: T
authors.initials: T
authors.lastname: Hata
authors.forename: T
authors.initials: T
authors.lastname: Maeda
authors.forename: M
authors.initials: M
authors.lastname: Honda
authors.forename: M
authors.initials: M
authors.lastname: Tawara
authors.forename: T
authors.initials: T
authors.lastname: Hayashibara
authors.forename: T
authors.initials: T
authors.lastname: Joh
authors.forename: M
authors.initials: M
authors.lastname: Tomonaga
authors.forename: Y
authors.initials: Y
authors.lastname: Miyazaki
authors.forename: S
authors.initials: S
authors.lastname: Kamihira
mesh_terms: D000911:Antibodies, Monoclonal / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology*; D015139:Blotting, Southern; D002352:Carrier Proteins / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D002999:Clone Cells; D053938:DNA Fragmentation / Q000187:drug effects; D018076:DNA, Complementary / Q000096:biosynthesis; D019008:Drug Resistance, Neoplasm; D015368:Human T-lymphotropic virus 1 / Q000235:genetics / Q000302:isolation & purification*; D006801:Humans; D015458:Leukemia, T-Cell / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000821:virology*; D054645:Protein Phosphatase 1; D054595:Protein Tyrosine Phosphatase, Non-Receptor Type 13; D017027:Protein Tyrosine Phosphatases / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014407:Tumor Cells, Cultured; D016662:Virus Integration / Q000235:genetics; D019014:fas Receptor / Q000276:immunology* / Q000494:pharmacology
chemical_list: D000911:Antibodies, Monoclonal; D002352:Carrier Proteins; D018076:DNA, Complementary; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D019014:fas Receptor; D054645:Protein Phosphatase 1; C516742:PTPN13 protein, human; D054595:Protein Tyrosine Phosphatase, Non-Receptor Type 13; D017027:Protein Tyrosine Phosphatases