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Higuchi T, Hannigan GE, Malkin D, et al. Enhancement by retinoic acid and dibutyryl cyclic adenosine 3':5'-monophosphate of the differentiation and gene expression of human neuroblastoma cells induced by interferon. Cancer Res. 1991;51(15):3958-64
Higuchi, T., Hannigan, G. E., Malkin, D., Yeger, H., & Williams, B. R. (1991). Enhancement by retinoic acid and dibutyryl cyclic adenosine 3':5'-monophosphate of the differentiation and gene expression of human neuroblastoma cells induced by interferon. Cancer research, 51(15), 3958-64.
Higuchi, T, et al. "Enhancement by retinoic acid and dibutyryl cyclic adenosine 3':5'-monophosphate of the differentiation and gene expression of human neuroblastoma cells induced by interferon." Cancer research vol. 51,15 (1991): 3958-64.
Higuchi T, Hannigan GE, Malkin D, Yeger H, Williams BR. Enhancement by retinoic acid and dibutyryl cyclic adenosine 3':5'-monophosphate of the differentiation and gene expression of human neuroblastoma cells induced by interferon. Cancer Res. 1991 Aug 01;51(15):3958-64. PMID: 1677311.
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Cancer Res. 1991 Aug 01;51(15):3958-64.

Enhancement by retinoic acid and dibutyryl cyclic adenosine 3':5'-monophosphate of the differentiation and gene expression of human neuroblastoma cells induced by interferon.

Cancer research

T Higuchi, G E Hannigan, D Malkin, H Yeger, B R Williams

Affiliations

  1. Division of Infectious Diseases, Hospital for Sick Children, Toronto, Ontario, Canada.

PMID: 1677311
Free Article

Abstract

Human neuroblastoma cell lines are induced to differentiate and display neuronal phenotypes when treated with interferon (IFN)-alpha 2, retinoic acid (RA), or dibutyryl cyclic AMP (dbcAMP). We investigated the effects of combinations of these agents in induction-differentiation in the neuroblastoma cell line, NUB-6. The inductive effect of IFN-alpha 2 was markedly enhanced when used in combination with RA or dbcAMP. In parallel, RA or dbcAMP also enhanced the level of 2'-5'-oligoadenylate (2-5A) synthetase, and enzyme induced by IFNs and implicated in their biological action. The levels of another IFN-inducible enzyme, p68 kinase, were not enhanced by the combination treatments. The enhancement effects appeared to be exerted largely at the posttranscriptional level as both RA and dbcAMP stabilized IFN-induced 2-5A synthetase mRNA, resulting in increased enzyme activity. Thus, the 2-5A synthetase system is likely involved in mediating the IFN-alpha 2-induced differentiation of neuroblastoma cells and may also mediate the enhancement effects of RA and dbcAMP on IFN activity in these cells. These results also provide a rational basis for establishing a combination therapeutic approach for the treatment of neuroblastoma.

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