Identity of differentiation inducing factor and tumour necrosis factor

Takeda, Ken; Iwamoto, Satoshi; Sugimoto, H.; Takuma, Tetsuo; Kawatani, Norika; Noda, Miki; Masaki, Atsushi; Morise, Hiroshi; Arimura, Hirofumi; Konno, Kunio

doi:10.1038/323338a0

Cited by 172 publications

(48 citation statements)

References 19 publications

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“…ML-1 cells which were derived from a patient with acute myeloblastic leukemia, are at an earlier stage of dierentiation than HL-60 cells and can be dierentiated easily into the macrophage but not the granulocytic pathway by various inducers such as tumor necrosis factor (Takeda et al, 1986), interferon-g (Takei et al, 1984) and 12-O-tetradecanoylphorbol-13-acetate (TPA) (Takeda et al, 1982;Saito et al, 1999). Retinoids generally do not promote granulocytic maturation in acute myeloid leukemia (AML) subtypes with the exception of acute promyelocytic leukemia (APL).…”

Section: Introductionmentioning

confidence: 99%

Complex regulation of CDKs and G1 arrest during the granulocytic differentiation of human myeloblastic leukemia ML-1 cells

2000

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We previously reported that all-trans retinoic acid (ATRA) and granulocyte-macrophage colony-stimulating factor (GM ± CSF) synergistically induced granulocytic dierentiation in human myeloblastic leukemia ML-1 cells. The combination of these agents also suppressed DNA-synthesis. In the present study, we investigated the suppression of cyclin dependent kinase (CDK) activities resulting in G1 arrest in dierentiated ML-1 cells. We show that treatment of ML-1 cells with ATRA plus GM-CSF results in G1 arrest and suppression of CDK activities. Protein levels of the G1 CDKs were essentially unchanged during this time. However, we observed an increase in CDK2-bound p27 and CDK4-bound p18, and a decrease in CDK6-bound cyclin D3. These results suggest that complex regulation of CDKs play a key role in G1 arrest of ML-1 after treatment with ATRA and GM ± CSF. We also showed that an increase in CDK2-bound p27 and CDK4-bound p18 are caused by treatment with ATRA and a decrease in CDK6-bound cyclin D3 is induced synergistically by treatment with both reagents. Furthermore, we propose that the changes in binding of p18 and cyclin D3 to CDKs are due to changes at the protein expression level and that the increase in p27 binding to CDK2 is due to a novel mechanism. Oncogene (2000) 19, 4640 ± 4646.

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Section: Introductionmentioning

confidence: 99%

Complex regulation of CDKs and G1 arrest during the granulocytic differentiation of human myeloblastic leukemia ML-1 cells

2000

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“…We (38). We have recently reported that tumor necrosis factor reduces directly and within 1 to 3 h the transcriptional rate of c-myc and that it cooperates with IFN to provide maximal c-myc inhibition (41).…”

Section: Discussionmentioning

confidence: 81%

Recessive genetic deregulation abrogates c-myc suppression by interferon and is implicated in oncogenesis.

Kimchi¹,

Resnitzky²,

Ber³

et al. 1988

Mol. Cell. Biol.

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In a previous study we demonstrated that many hematopoietic tumor cells are resistant to the inhibitory effects that interferon exerts on c-myc mRNA expression without losing other receptor-mediated intracellular responses (M. Einat, D. Resnitzky, and A. Kimchi, Nature [London] 313:597400). We report here that this partial resistance was overridden in two independent stable somatic cell hybrids prepared by fusion between sensitive and resistant cells. The c-myc mRNA transcribed from the active allele of the resistant parent cell was reduced by interferon within the context of the cell hybrid. It was therefore concluded that changes in the cis-acting sequences of c-myc were not involved in this type of relaxed regulation and that resistance resulted rather from inactivation or loss of postreceptor elements which operate in trans. The growth-stimulating effect that this genetic deregulation might have on cells was tested in experimental systems of cell differentiation in which an autocrine interferon is produced. For that purpose we isolated variant clones of Ml myeloid cells which were partially resistant to alpha and beta interferons and tested their growth behavior during in vitro-induced differentiation. The resistant clones displayed higher proliferative activity on days 2 and 3 of differentiation than did the sensitive clones, which stopped proliferating. The loss of c-myc responses to the self-produced interferon disrupted the normal cessation of growth during differentiation and therefore might lead cells along the pathway of neoplasia.

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“…Recently, Takeda et al demonstrated that a DIF purified from the culture supernatant of phytohemagglutinin-stimulated leukocytes is identical to TNF (37). TNF is also released by lymphocytes and HUT-102 cells when stimulated with phorbol esters and calcium ionophore (7,21).…”

Section: Discussionmentioning

confidence: 99%

Purification and Characterization of a T Lymphocyte‐Derived Differentiation‐Inducing Factor for Human Promyelocytic Cell Line (HL‐60) and Its Relationship to Lymphotoxin

Shimizu

Nakamura

Niki

et al. 1989

Microbiology and Immunology

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The human T cell leukemia virus type I (HTLV-I)-transformed T lymphocyte cell line MT-2 constitutively produces differentiation-inducing factor (DIF) for the human promyelocytic leukemia cell line HL-60. Purification and characterization of DIF derived from MT-2 were performed here to identify T cell-derived DIF. DIF was purified from conditioned medium of the MT-2 cell culture with serum-free medium by utilizing the sequential chromatographies of anion-exchange (mono-Q) column, gel filtration (superose-12) column, and hydrophobic (phenyl 5PW) column and finally the sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). In the SDS-PAGE, one major band with a molecular weight of 56,000 and one minor band with 15,000 were stained with Coomassie Brilliant Blue and both showed DIF activity after extraction from gels. DIF had an isoelectric point of 5.8. In all purification steps, DIF activity for HL-60 and cytotoxic activity to the sublines of mouse L-929 were not able to be separated. Further, DIF was neutralized by antibody against lymphotoxin (LT) but not by antibody against tumor necrosis factor. These results indicate that the major DIF activity derived from MT-2 is LT.In recent years, the development of human leukemia cell lines has provided useful models for studying proliferation and differentiation of hematopoietic cells. The human promyelocytic leukemia cell line HL-60 (6) is induced to differentiate 'rPresent addresses:

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Identity of differentiation inducing factor and tumour necrosis factor

Cited by 172 publications

References 19 publications

Complex regulation of CDKs and G1 arrest during the granulocytic differentiation of human myeloblastic leukemia ML-1 cells

Complex regulation of CDKs and G1 arrest during the granulocytic differentiation of human myeloblastic leukemia ML-1 cells

Recessive genetic deregulation abrogates c-myc suppression by interferon and is implicated in oncogenesis.

Purification and Characterization of a T Lymphocyte‐Derived Differentiation‐Inducing Factor for Human Promyelocytic Cell Line (HL‐60) and Its Relationship to Lymphotoxin

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