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Blood, 1 July 2004, Vol. 104, No. 1, pp. 237-242.
Prepublished online as a Blood First Edition Paper on March 16, 2004; DOI 10.1182/blood-2003-07-2203.
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NEOPLASIA
Insulin-like growth factor binding protein-3 antagonizes the effects of retinoids in myeloid leukemia cells
Takayuki Ikezoe,
Sakae Tanosaki,
Utz Krug,
Bingrong Liu,
Pinchas Cohen,
Hirokuni Taguchi, and
H. Phillip Koeffler
From the Division of Hematology/Oncology, Cedars-Sinai Medical Center, Pediatric Endocrinology, University of California at Los Angeles School of Medicine, Los Angeles, CA; and the Department of Internal Medicine, Kochi Medical School, Kochi, Japan.
Insulin-like growth factor binding protein-3 (IGFBP-3) can cause growth suppressive and proapoptotic effects on retinoids in many types of cancer cells. However, the expression and effects of IGFBP-3 in myeloid leukemia cells have not been elucidated. In this study, we found no IGFBP-3 expression in the human myeloid leukemia cell lines either at baseline or after stimulation with all-trans retinoic acid (ATRA). Human recombinant IGFBP-3 induced growth arrest and apoptosis of HL-60 and NB4 cells. We have previously identified RXR as a nuclear receptor for IGFBP-3 and have proceeded to examine further the role of this interaction in leukemia cell lines. In signaling assays, IGFBP-3 potently suppressed RAR- and VDR-mediated signaling while enhancing RXR signaling. Interestingly, when IGFBP-3 was administered to these cells in combination with an RAR-selective ligand, the ability of these retinoids to induce differentiation was blunted. On the other hand, IGFBP-3 enhanced the effect of an RXR-selective ligand to induce differentiation of HL-60 and NB4 cells. Further studies showed that IGFBP-3 down-regulated (at the transcriptional level) the retinoid-induced expression of C/EBP in NB4 cells. Taken together, these results indicate that IGFBP-3 has antiproliferative activity against myeloid leukemia cells; while it enhances signaling through RXR/RXR, it blunts signaling by activated RAR/RXR.
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