Antiproliferative effect of retinoid compounds on Kaposi's sarcoma cells.

Corbeil, Jacques; Rapaport, Eric; Richman, Douglas D.; Looney, David J.

doi:10.1172/jci117190

Cited by 55 publications

(22 citation statements)

References 36 publications

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“…The prominent effect of ATRA on this type of tumor, however, depended on the ability of ATRA to directly inhibit the function of the PML-RXRa oncoprotein and was not necessarily related to its redifferentiation property [19]. Experimental studies report growth-inhibitory effects on osteosarcoma [47], rhabdomyosarcoma [40], and AIDS-associated Kaposi sarcoma [15]. Approximately 30% of patients with AIDSassociated Kaposi sarcoma have a substantial clinical response to ATRA treatment [8], and one case report suggested ATRA treatment combined with interferon-a was effective against inoperable metastatic osteosarcoma [48].…”

Section: Discussionmentioning

confidence: 99%

Neuronal Differentiation of Synovial Sarcoma and Its Therapeutic Application

Ishibe

Nakayama

Aoyama

et al. 2008

Clin Orthop Relat Res

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Synovial sarcoma is a rare sarcoma of unknown histologic origin. We previously reported the gene expression profile of synovial sarcoma was closely related to that of malignant peripheral nerve sheath tumors, and the fibroblast growth factor (FGF) signal was one of the main growth signals in synovial sarcoma. Here we further demonstrate the neural origin of synovial sarcoma using primary tumors and cell lines. The expression of neural tissuerelated genes was confirmed in synovial sarcoma tumor tissues, but the expression of some genes was absent in synovial sarcoma cell lines. Treatment of synovial sarcoma cell lines with BMP4 or FGF2 enhanced or restored the expression of neural tissue-related genes and induced a neuron-like morphology with positive Tuj-1 expression. Treatment with all-trans-retinoic acid also induced the expression of neural tissue-related genes in association with growth inhibition, which was not observed in other cell lines except a malignant peripheral nerve sheath tumor cell line. A growth-inhibitory effect of all-trans-retinoic acid was also observed for xenografted tumors in athymic mice. The simultaneous treatment with FGF signal inhibitors enhanced the growth-inhibitory effect of all-trans-retinoic acid, suggesting the combination of growth signaling inhibition and differentiation induction could be a potential molecular target for treating synovial sarcoma.

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Section: Discussionmentioning

confidence: 99%

Neuronal Differentiation of Synovial Sarcoma and Its Therapeutic Application

Ishibe

Nakayama

Aoyama

et al. 2008

Clin Orthop Relat Res

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“…Retinoids-induce apoptosis in myeloid leukemia cells (Martin et al, 1990), neuroblastoma cells (Melino et al, 1994), breast (Seewald et al, 1995), ovarian (Krupitza et al, 1995) and cervical cancer cells (Oridate et al, 1995) and many other types of cells (Atencia et al, 1994;Corbeil et al, 1994;Kalemkerian et al, 1995;Nakamura et al, 1995). In many of these systems ligands that activate particular subsets of RARs have proven to be particularly efficacious.…”

Section: Retinoid Receptors and Apoptosismentioning

confidence: 99%

Retinoid-induced apoptosis in normal and neoplastic tissues

Thomázy²,

et al. 1998

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Vitamin A and its derivatives (collectively referred to as retinoids) are required for many fundamental life processes, including vision, reproduction, metabolism, cellular differentiation, hematopoesis, bone development, and pattern formation during embryogenesis. There is also considerable evidence to suggest that natural and synthetic retinoids have therapeutical effects due to their antiproliferative and apoptosis-inducing effectsin human diseases such ascancer. Therefore it is not surprising that a significant amount of research was dedicated to probe the molecular and cellular mechanisms of retinoid action during the past decade. One of the cellular mechanisms retinoids have been implicated in is the initiation and modulation of apoptosis in normal development and disease. This review provides a brief overview of the molecular basis of retinoid signaling, and focuses on the retinoid-regulation of apoptotic cell death and gene expression during normal development and in pathological conditions in vivo and in various tumor cell lines in vitro.Keywords: retinoic acid; retinoic acid receptor; RAR; RXR; apoptosis; tissue transglutaminase; gene expression Abbreviations: ATRA, All-trans retinoic acid; 9-cis RA, 9-cis retinoic acid; PG-J 2 , 15-deoxy-D 12,14 PGJ 2 ; RAR, retinoic acid receptor; RXR, retinoid X receptor; Tgase, tissue transglutaminase; SMRT, silencing mediator of retinoid and thyroid receptors; N-CoR, nuclear receptor corepressor; CREB, creb binding protein; HDAC-1, histone deacetylase-1 Retinoids are modulators of transcriptionThe retinoid's mechanism of action in both normal and pathological conditions has been the subject of more than a decade of intense research. The cloning and discovery of the retinoic acid receptor (RAR), which belongs to the superfamily of ligand-activated transcription factors (nuclear receptors) revolutionized our understanding as to how retinoids exert their pleiotropic effects (for reviews see Chambon (1996);Mangelsdorf et al (1994)). Members of the nuclear receptor superfamily mediate the biological effects of many hormones, vitamins and drugs (i.e. steroid hormones, thyroid hormones, vitamin D, prostaglandin-J 2 (PG-J 2 ) and drugs that activate peroxisomal proliferation). There are two families of retinoid receptors, Retinoid X Receptors (RXRs) that bind 9-cis retinoic acid (9-cis RA) and Retinoic Acid Receptors (RARs) that bind both 9-cis RA and all-trans retinoic acid (ATRA) (for reviews see Chambon 1996;Mangelsdorf et al, 1994)). Each of these receptor families includes at least three distinct genes, (RARa,b and g; RXRa,b and g) that through differential promoter usage and alternative splicing, give rise to a large number of distinct retinoid receptor proteins (for reviews see

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“…2), thus suggesting that the RXR signal transduction pathway is operational only in transfected HeLa cells but not in untransfected KS cells. (3,9,18). In the present study, we demonstrate that retinoids inhibit KS cell growth in culture by inhibiting IL-6 protein, which is an autocrine growth factor for KS cells (29).…”

Section: Retinoid-dependent Inhibition Of Nf-il6-mediated Expression mentioning

confidence: 99%

“…Human immunodeficiency virus tat protein is also a mitogen for KS cells and a comitogen for human umbilical vein endothelial cells (12). Retinoids exert antiproliferative and differentiating activity in a variety of normal and tumor cells (9). Retinoic acid (RA) is known to regulate IL-6 (39) and has produced tumor responses in KS (3,18).…”

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confidence: 99%