The c-fes protooncogene is expressed at high levels in the terminal stages of granulocytic differentiation, but so far no definite function has been attributed to the product of this oncogene. To tackle this problem, the c-fes protooncogene expression has been inhibited in HL60 cells, and fresh leukemic promyelocytes of acute promyelocytic leukemia have been induced to differentiate with retinoic acid (RA) and dimethylsulfoxide (DMSO). Inhibition was obtained by incubating the cells with a specific c-fes antisense oligodeoxynucleotide. It was observed that the cells, rather than differentiating, underwent premature cell death showing the morphological and molecular characteristics of apoptosis. This process was inhibited by granulocyte and granulocyte/macrophage colony-stimulating factor, but not by interleukin 3 (IL-3), IL-6, or stem cell factor. Our present results demonstrate that the loss of cell viability that occurs during the in vitro differentiation of myeloid cells, after the complete inhibition of the c-fes gene product and treatment with RA-DMSO, is due to activation of programmed cell death. It is concluded that a possible role of the c-fes gene product is to exert an antiapoptotic effect during granulocytic differentiation.

Inhibition of c-fes expression by an antisense oligomer causes apoptosis oh HL60 cells induced to granulocytic differentiation / Manfredini, Rossella; Grande, Alexis; Tagliafico, Enrico; D., Barbieri; P., Zucchini; G., Citro; G., Zupi; C., Franceschi; U., Torelli; Ferrari, Sergio. - In: JOURNAL OF EXPERIMENTAL MEDICINE. - ISSN 0022-1007. - STAMPA. - 178:(1993), pp. 381-389.

Inhibition of c-fes expression by an antisense oligomer causes apoptosis oh HL60 cells induced to granulocytic differentiation

MANFREDINI, Rossella;GRANDE, Alexis;TAGLIAFICO, Enrico;FERRARI, Sergio
1993-01-01

Abstract

The c-fes protooncogene is expressed at high levels in the terminal stages of granulocytic differentiation, but so far no definite function has been attributed to the product of this oncogene. To tackle this problem, the c-fes protooncogene expression has been inhibited in HL60 cells, and fresh leukemic promyelocytes of acute promyelocytic leukemia have been induced to differentiate with retinoic acid (RA) and dimethylsulfoxide (DMSO). Inhibition was obtained by incubating the cells with a specific c-fes antisense oligodeoxynucleotide. It was observed that the cells, rather than differentiating, underwent premature cell death showing the morphological and molecular characteristics of apoptosis. This process was inhibited by granulocyte and granulocyte/macrophage colony-stimulating factor, but not by interleukin 3 (IL-3), IL-6, or stem cell factor. Our present results demonstrate that the loss of cell viability that occurs during the in vitro differentiation of myeloid cells, after the complete inhibition of the c-fes gene product and treatment with RA-DMSO, is due to activation of programmed cell death. It is concluded that a possible role of the c-fes gene product is to exert an antiapoptotic effect during granulocytic differentiation.
178
381
389
Inhibition of c-fes expression by an antisense oligomer causes apoptosis oh HL60 cells induced to granulocytic differentiation / Manfredini, Rossella; Grande, Alexis; Tagliafico, Enrico; D., Barbieri; P., Zucchini; G., Citro; G., Zupi; C., Franceschi; U., Torelli; Ferrari, Sergio. - In: JOURNAL OF EXPERIMENTAL MEDICINE. - ISSN 0022-1007. - STAMPA. - 178:(1993), pp. 381-389.
Manfredini, Rossella; Grande, Alexis; Tagliafico, Enrico; D., Barbieri; P., Zucchini; G., Citro; G., Zupi; C., Franceschi; U., Torelli; Ferrari, Sergio
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/310803
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