Induction of TrkB by retinoic acid mediates biologic responsiveness to BDNF and differentiation of human neuroblastoma cells

Kaplan, David R.; Matsumoto, Kazue; Lucarelli, Enrico; Thielet, Carol J.

doi:10.1016/0896-6273(93)90187-v

Cited by 307 publications

(273 citation statements)

References 50 publications

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“…Combining our own present and previous results (Kogner et al, 1993) with those from other groups (Borello et al, 1993;Kaplan et al, 1993;Matsumoto et al, 1995;Nakagawara et al, 1994;Suzuki et al, 1993) a specific pattern of neurotrophin receptor expression in various neuroblastoma tumours emerges. Favourable neuroblastoma tumours express trkA together with p75LNGFR and sometimes full-length trkC, but only truncated trkB.…”

supporting

confidence: 85%

“…It was recently suggested that neurotrophic factors could be provided to differentiating tumour cells by infiltrating normal Schwann cells that can often be found in maturing NB (Ambros and Ambros, 1995). NGF and its receptors are suggested to play a part in tumour differentiation and regression or apoptosis (Matsushima and Bogenmann, 1993;Nakagawara et al, 1993;Poluha et al, 1995) while the trkB-BDNF autocrine loop has been proposed to support tumour survival and invasiveness (Kaplan et al, 1993;Matsumoto et al, 1995;Nakagawara et al, 1994 …”

mentioning

confidence: 99%

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Expression of mRNA for the neurotrophin receptor trkC in neuroblastomas with favourable tumour stage and good prognosis

Rydén

Sehgal²,

Dominici³

et al. 1996

Br J Cancer

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(RT-PCR) showed that mRNA encoding the full-length cytoplasmic tyrosine kinase domain of the receptor was only expressed in a subset of favourable tumours. These data show that favourable neuroblastomas may express the full trkC receptor while advanced tumours, in particular MYCN-amplified neuroblastoma, seem to either express no trkC or truncated trkC receptors of as yet unknown biological function. These data are suggestive of a role for trkC and its preferred ligand neutotrophin-3, NT-3, in neuroblastoma differentiation and/or regression.

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supporting

confidence: 85%

mentioning

confidence: 99%

Expression of mRNA for the neurotrophin receptor trkC in neuroblastomas with favourable tumour stage and good prognosis

Rydén

Sehgal²,

Dominici³

et al. 1996

Br J Cancer

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“…the PC12 cell line and NGF; reviewed Kaplan and Stephens, 1994: neuroblastoma cell lines and BDNF; Kaplan et al, 1993). Dev cells respond to FGF2 in a manner which is extremely similar to that described for pluripotent stem cells and multipotent precursors.…”

Section: Discussionmentioning

confidence: 85%

Human primitive neuroectodermal tumour cells behave as multipotent neural precursors in response to FGF2

Dufay

Rudkin

et al. 1998

Oncogene

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Primitive neuroectodermal tumours (PNET) are thought to derive from the malignant transformation of pluripotent CNS precursors although this hypothesis has yet to be tested in vitro. Here we show that cells of a human PNET cell line`Dev' express functional ®broblast growth factor (FGF) receptors (FGFR) and respond to FGF2 as multipotent CNS precursors. FGF2 induces tyrosine phosphorylation of FGFR-1 and FGFR-2 and many cellular substrates including MAP kinases and stimulates proliferation. Cells detach from plastic substrates and proliferate to form large clusters of undi erentiated cells. After adhesion to polylysine, cells migrate out from the clusters and di erentiate. The majority of di erentiated cells express neuronal phenotypes but distinct subpopulations express oligodendrocytic and astrocytic markers. Mature neural di erentiation markers are not otherwise detected in Dev cells in de®ned medium. Identical results were obtained with 12 monoclonal subclones as well as the parent cell line, con®rming that Dev cells are multipotent. This extends evidence that multipotent CNS precursors are the cellular substrate from which certain PNET develop and shows that FGF2 is a potent proliferation and di erentiation inducer for PNET cells in vitro, suggesting that FGF2 may also modulate the evolution of PNET in vivo. Finally our results suggest that PNET cell lines may provide models to elucidate the biology of human multipotent CNS precursors.

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“…Our results show that stimulation of PKC or Ras/MAPK which elicit an arrest in cell growth and promote maturation in these cells converges with the actions of retinoids to activate RARb gene transcription providing an example of cross talk among di erent signaling pathways. An inhibition of expression of N-myc in cells with this oncogene ampli®ed (Thiele et al, 1985), or the induction of TrkB, a tyrosine kinase receptor known to be important in neuron survival and di erentiation, may be some of the mechanisms by which RA subsequently causes neuroblastoma cell maturation (Kaplan et al, 1993;Nakagawara et al, 1994). Retinoids have proven to be of clinical use in the treatment of di erent tumors.…”

Section: Discussionmentioning

confidence: 99%

Differentiation of neuroblastoma cells by phorbol esters and insulin-like growth factor 1 is associated with induction of retinoic acid receptor β gene expression

Pérez-Juste

Aranda

1999

Oncogene

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The retinoic acid (RA) receptor b isoform (RARb) plays an important role in RA-induced di erentiation of human neuroblastoma. In this study we show that insulin-like growth factor 1 (IGF-1) and tetradecanoyl phorbol acetate (TPA) induce RARb gene expression in neuroblastoma SH-SY5Y cells. IGF-1 and TPA caused a marked induction of RARb2 promoter activity and had a synergistic e ect with RA that also upregulates transcription. The e ect of RA is mediated by two RA responsive elements (RAREs), whereas the IGF-1 and TPA actions are independent of the RAREs and map to sequences that overlap the TATA box. These results suggest that the signaling pathways stimulated by TPA and IGF-1 could modify the components assembled at the core RARb2 promoter and activate transcription. Expression of Ras Val12 mimics the e ect of IGF-1 and TPA on the promoter, and a dominant negative Ras mutant abrogates activation. A dominant negative Raf also blocks activation showing that the Ras-Raf pathway mediates stimulation of the RARb2 promoter. Our results show that neuronal di erentiation induced by non-retinoid agents that activate Ras is accompanied by increased transcription of the RARb gene.

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Induction of TrkB by retinoic acid mediates biologic responsiveness to BDNF and differentiation of human neuroblastoma cells

Cited by 307 publications

References 50 publications

Expression of mRNA for the neurotrophin receptor trkC in neuroblastomas with favourable tumour stage and good prognosis

Expression of mRNA for the neurotrophin receptor trkC in neuroblastomas with favourable tumour stage and good prognosis

Human primitive neuroectodermal tumour cells behave as multipotent neural precursors in response to FGF2

Differentiation of neuroblastoma cells by phorbol esters and insulin-like growth factor 1 is associated with induction of retinoic acid receptor β gene expression

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