title: Interleukin-1alpha regulates G1 cell cycle progression and arrest in thyroid carcinoma cell lines NIM1 and NPA.
abstract: This study provides the first report that the same cytokine (interleukin-1 (IL-1)) can induce opposite effects on cyclin-dependent kinases (Cdks) and Cdk inhibitors (Cdkis) in the G1 phase even in the same type of cancer cells (papillary thyroid carcinoma cells). Cell cycle analysis revealed an increase in NIM1 cells and a decrease in NPA cells in the S and G2+M phases after treatment with IL-1alpha. The addition of IL-1alpha to NIM1 cells reduced the expression of p16 and p21 protein and induced the expression of Cdk2 and Cdk4 protein, which leads to the phosphorylation of retinoblastoma protein. The addition of IL-1alpha to NPA cells induced the expression of p27 protein and reduced the expression of Cdk2 protein, which leads to induction of p107 protein expression. It is of interest that p21 protein expression was not observed in NPA cells. These results suggest that several Cdks and Cdkis play a regulatory role in the G1 cell cycle progression and arrest induced by IL-1alpha in thyroid carcinoma cell lines.
authors.affiliation: First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Zeki
authors.forename: I
authors.initials: I
authors.lastname: Morimoto
authors.forename: T
authors.initials: T
authors.lastname: Arao
authors.forename: S
authors.initials: S
authors.lastname: Eto
authors.forename: U
authors.initials: U
authors.lastname: Yamashita
mesh_terms: D015153:Blotting, Western; D042846:CDC2-CDC28 Kinases; D002291:Carcinoma, Papillary / Q000378:metabolism / Q000473:pathology*; D018797:Cell Cycle Proteins / Q000032:analysis*; D051357:Cyclin-Dependent Kinase 2; D051358:Cyclin-Dependent Kinase 4; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000032:analysis; D018844:Cyclin-Dependent Kinases / Q000032:analysis / Q000037:antagonists & inhibitors / Q000378:metabolism*; D004247:DNA / Q000032:analysis; D004268:DNA-Binding Proteins / Q000032:analysis; D016193:G1 Phase; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D007375:Interleukin-1 / Q000032:analysis / Q000494:pharmacology*; D008840:Microfilament Proteins / Q000032:analysis; D009124:Muscle Proteins; D009687:Nuclear Proteins / Q000032:analysis; D017346:Protein Serine-Threonine Kinases / Q000032:analysis; D011518:Proto-Oncogene Proteins; D016160:Retinoblastoma Protein / Q000032:analysis; D050720:Retinoblastoma-Like Protein p107; D013964:Thyroid Neoplasms / Q000378:metabolism / Q000473:pathology*; D014157:Transcription Factors / Q000032:analysis; D014407:Tumor Cells, Cultured
chemical_list: D018797:Cell Cycle Proteins; D019941:Cyclin-Dependent Kinase Inhibitor p16; D004268:DNA-Binding Proteins; D007375:Interleukin-1; D008840:Microfilament Proteins; D009124:Muscle Proteins; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; C493844:RBL1 protein, human; C489485:Rbl1 protein, mouse; D016160:Retinoblastoma Protein; D050720:Retinoblastoma-Like Protein p107; C087628:TCEAL1 protein, human; C058992:Tagln protein, mouse; D014157:Transcription Factors; D004247:DNA; D017346:Protein Serine-Threonine Kinases; D042846:CDC2-CDC28 Kinases; C495894:CDK2 protein, human; C495900:CDK4 protein, human; D051357:Cyclin-Dependent Kinase 2; D051358:Cyclin-Dependent Kinase 4; D018844:Cyclin-Dependent Kinases