Abstract
In HL-60 cells, a human promyelocytic leukemia cell line, the human c-myc gene, designated MYC, is amplified about 16-fold. On differentiation of the HL-60 cells into granulocytes induced by several inhibitors of poly(ADP-ribose) polymerase [NAD+ poly(adenosine diphosphate D-ribose)ADP-D-ribosyltransferase, EC 2.4.2.30] including benzamide, nicotinamide, coumarin, and 4-hydroxyquinazoline or dimethyl sulfoxide, some MYC loss was observed. In contrast, benzoic acid, a noninhibitory analogue of benzamide, did not induce either granulocytic differentiation or loss of MYC. Loss of MYC seems to be associated with granulocytic differentiation because the time course of its loss was similar to that of appearance of nitroblue tetrazolium-positive cells, mature granulocytes, and its loss was not observed on differentiation of HL-60 cells into macrophages induced by phorbol 12-myristate 13-acetate or teleocidin. The loss of MYC is not the reason for the down regulation of MYC expression observed within 1 hr after addition of inducers, since the loss of MYC was not detected by 1-day treatment with inducers.
MeSH Terms
Benzamides/pharmacology
Blotting, Southern
Cell Differentiation/drug effects
Cell Line
Coumarins/pharmacology
Dimethyl Sulfoxide/pharmacology
Gene Amplification
Humans
Leukemia, Promyelocytic, Acute/genetics
Niacinamide/pharmacology
Nucleic Acid Hybridization
Poly(ADP-ribose) Polymerase Inhibitors
Proto-Oncogene Proteins/genetics
Proto-Oncogene Proteins c-myc
Proto-Oncogenes/drug effects
Quinazolines/pharmacology
Quinazolinones
RNA, Neoplasm/drug effects,genetics
Chemicals
Benzamides
Coumarins
Poly(ADP-ribose) Polymerase Inhibitors
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-myc
Quinazolines
Quinazolinones
RNA, Neoplasm
Niacinamide
benzamide
4-hydroxyquinazoline
coumarin
Dimethyl Sulfoxide
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Shima H
Carcinogenesis Division, National Cancer Center Research Institute, Tokyo, Japan.
Nakayasu M
Aonuma S
Sugimura T
Nagao M
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