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Research Article Free access | 10.1172/JCI116062

Induction of thrombospondin 1 by retinoic acid is important during differentiation of neuroblastoma cells.

V P Castle, X Ou, S O'Shea, and V M Dixit

Department of Pediatrics, University of Michigan Medical School, Ann Arbor 48109.

Find articles by Castle, V. in: PubMed | Google Scholar

Department of Pediatrics, University of Michigan Medical School, Ann Arbor 48109.

Find articles by Ou, X. in: PubMed | Google Scholar

Department of Pediatrics, University of Michigan Medical School, Ann Arbor 48109.

Find articles by O'Shea, S. in: PubMed | Google Scholar

Department of Pediatrics, University of Michigan Medical School, Ann Arbor 48109.

Find articles by Dixit, V. in: PubMed | Google Scholar

Published November 1, 1992 - More info

Published in Volume 90, Issue 5 on November 1, 1992
J Clin Invest. 1992;90(5):1857–1863. https://doi.org/10.1172/JCI116062.
© 1992 The American Society for Clinical Investigation
Published November 1, 1992 - Version history
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Abstract

Neuroblastoma, a malignant neoplasm that arises in the adrenal medulla or sympathetic ganglion, is one of the most common solid tumors of childhood. Reports that neuroblastomas spontaneously mature to form benign ganglioneuromas have prompted investigations into the efficacy of using agents that induce neuronal differentiation in the treatment of this malignancy. Retinoic acid is one agent in particular that has been shown to induce growth inhibition and terminal differentiation of neuroblastoma cell lines in vitro. Using the human neuroblastoma cell line SMH-KCNR, we have investigated the role of the extracellular matrix protein thrombospondin in retinoic acid induced neuroblastoma differentiation. Treatment with retinoic acid results in a rapid induction (within 4 h) of thrombospondin (TSP) message which is independent of intervening protein synthesis and superinducible in the presence of cycloheximide. This suggests that TSP functions as a retinoic acid inducible immediate early response gene. A concomitant increase in both cell associated and soluble forms of TSP protein can be detected within 24 h of retinoic acid treatment. A functional role for TSP in SMH-KCNR differentiation was established in experiments which showed that exposure to anti-TSP monoclonal antibodies delay retinoic acid differentiation for 48 h. At the time the cells overcome the effects of TSP inhibition, laminin production becomes maximal. Treatment of the cells with a combination of anti-TSP and antilaminin antibodies results in complete inhibition of differentiation.

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