Matrix metalloproteinases expression in HL-60 promyelocytic leukemia cells during apoptosis

被引：0
作者：
G. Gazzanelli
F. Luchetti
S. Burattini
F. Mannello
E. Falcieri
S. Papa
机构：
[1] Università degli Studi,Istituto di Istologia ed Analisi di Laboratorio, Facoltà di Scienze MFN
[2] Centro di Citometria e Citomorfologia,Istituto di Istologia ed Analisi di Laboratorio, Facoltà di Scienze MFN
[3] Campus Scientifico,undefined
[4] Loc. Crocicchia,undefined
[5] Istituto di Scienze Morfologiche,undefined
[6] Campus Scientifico,undefined
[7] Loc. Crocicchia,undefined
[8] Università degli Studi,undefined
来源：
Apoptosis | 2000年 / 5卷
关键词：
Apoptosis; HL-60 cells; electron microscopy; matrix metalloproteinases;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
Human promyelocytic leukemia HL-60 cells have been used as a model to study both the expression of matrix-metalloproteinases and the mechanisms of programmed cell death. In the present study we examined the expression of these proteases in HL-60 cells stimulated by different apoptotic triggers. As shown by zymography, HL-60 cells released three major isofroms of the matrix-degrading proteases; when the leukemic cells were grown in serum-free conditions, as well as after hyperthermia and methotrexate treatment, we found a significant loss of the constitutive production of the 92 kDa matrix-metalloprotease, with an unequivocable molecular and ultrastructural evidence of programmed cell death. These results suggest that in HL-60 cells the expression/release of matrix metalloproteases can be down-regulated in the presence of the apoptotic-induced alterations, and that the decreased matrix-degrading capacity of this leukemic cell line during apoptosis may reduce its invasive potential.
引用
收藏
页码：165 / 172
页数：7
相关论文
共 89 条
  • [1] Chambers AF(1997)Changing view of the role of matrix metalloproteinases in metastasis J Natl Cancer Inst 89 1260-1270
  • [2] Matrisian LM.(1991)Neutral proteinases of human mononuclear phagocytes: cellular differentiation markedly alters cell phenotype for serine proteinases, metalloproteinases and tissue inhibitor of metalloproteinases J Immunol 146 1286-1293
  • [3] Campbell EJ(1996)TNF-alpha and IL-1 beta selectively induce expression of 92–kDa gelatinases by human macrophages J Immunol 157 4159-4165
  • [4] Cury JD(1989)The HL-60 promyelocytic leukemia cell line: proliferation, differentiation and cellular oncogene expression Blood 70 1233-1244
  • [5] Shapiro SD(1994)Use of the Matrigel-based assay to measure the invasiveness of leukemic cells Exp Hematol 22 559-565
  • [6] Saren P(1996)Matrix metalloproteinases and tumor invasion: from correlation and casuality to the clinic Semin Cancer Biol 7 147-159
  • [7] Welgus HG(1994)Regulation of 92–kD gelatinase in the HL-60 leukemia cells: tumor necrosis factor-alpha as an autocrine stimulus for basal-and phorbol ester-induced secretion Blood 83 3638-3646
  • [8] Kovanen PT.(1997)Production and activation of matrix metalloprotease-9 by HL-60 promyelocytic leukemia cells Biochem Biophys Res Commun 238 842-846
  • [9] Collins SJ.(1998)Autocrine regulation of macrophage differentiation and 92–kDa gelatinase production by tumor necrosis factor-alpha via alpha5 beta1 integrin in HL-60 cells J Biol Chem 273 11583-11588
  • [10] Janiak M(1999)Expression of matrix metalloproteinases (MMP-2 and-9) and tissue inhibitors of metalloproteinases (TIMP-1 and-2) in acute myelogenous leukemia blasts: comparison with normal bone marrow cells Br J Haematol 105 402-411
123456789