Selective Usage of D-Type Cyclins by Ewing’s Tumors and Rhabdomyosarcomas

Zhang, Jingsong; Hu, Siwen; Schofield, Deborah E.; Sorensen, Poul H.; Triche, Timothy J.

doi:10.1158/0008-5472.can-03-2594

Cited by 57 publications

(53 citation statements)

References 55 publications

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“…Also, a recent study has demonstrated distinct regulation of D-type cyclins in Ewing tumor cells; in TC-71 Ewing sarcoma cells, inhibition of EWSFli1 decreases the level of cyclin D1 but increases that of cyclin D3 (43). However, in TC-135 cells, we showed that cyclin D3 expression was down-regulated by transfection with EWS-Fli1 siRNA.…”

Section: The Relationship Between Ews-fli1 and Pld Expression In Cellcontrasting

confidence: 51%

“…The Effect of cyclin D Expression on Ewing Sarcoma CellsSome previous studies have shown that EWS-Fli1 is correlated with cyclin D expression (43)(44)(45)(46). Also, a recent study has demonstrated distinct regulation of D-type cyclins in Ewing tumor cells; in TC-71 Ewing sarcoma cells, inhibition of EWSFli1 decreases the level of cyclin D1 but increases that of cyclin D3 (43).…”

Section: The Relationship Between Ews-fli1 and Pld Expression In Cellmentioning

confidence: 98%

“…The reason for the difference in cyclin D3 expression between these two cell lines remains to be elucidated. Furthermore, cell-and tissue-specific patterns of D-type cyclin expression have been reported (43). In Ewing tumors and rhabdomyosarcomas, both the Ras-ERK and PI3K-Akt pathways regulate cyclin D expression (43).…”

Section: The Relationship Between Ews-fli1 and Pld Expression In Cellmentioning

confidence: 99%

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Inhibition of Platelet-derived Growth Factor-induced Cell Growth Signaling by a Short Interfering RNA for EWS-Fli1 via Down-regulation of Phospholipase D2 in Ewing Sarcoma Cells

Nozawa¹,

Ohno²,

Banno

et al. 2005

Journal of Biological Chemistry

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EWS-Ewing sarcoma and other peripheral primitive neuroectodermal tumors are pediatric malignant solid tumors, Ͼ95% of which show the chromosomal translocations t(11;22, q24;q12) or t(21;22, q22;q12), which produce the fusion genes EWS-Fli1 and EWS-erg, respectively (1-4). Cytogenetic and molecular analyses of these translocation products have revealed that the 5Ј-region of the EWS gene (from band 22q12) is fused to the 3Ј-region of either the Fli-1 gene (from band 11q24) or the erg gene (from band 21q22), both of which are members of the ETS family of transcription factors. Less frequent chromosomal translocations involve the same region of the EWS gene and various other ETS genes, such as ETV-1, E1AF, or FEV (1, 2). We have previously shown that EWS preferentially binds to poly(G) and poly(U) RNA. The binding activity of EWS is located in the RGG box, which is in the carboxyl-terminal region.

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Section: The Relationship Between Ews-fli1 and Pld Expression In Cellcontrasting

confidence: 51%

Section: The Relationship Between Ews-fli1 and Pld Expression In Cellmentioning

confidence: 98%

Section: The Relationship Between Ews-fli1 and Pld Expression In Cellmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of Platelet-derived Growth Factor-induced Cell Growth Signaling by a Short Interfering RNA for EWS-Fli1 via Down-regulation of Phospholipase D2 in Ewing Sarcoma Cells

Nozawa¹,

Ohno²,

Banno

et al. 2005

Journal of Biological Chemistry

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“…In addition, as mentioned above, forced expression of RAGE in TE671 cells results in down-regulation of expression of cyclin D1 ( Figure 5I), which is overexpressed in highly proliferating, metastatic cells, including RMS cells, has an important role in cellular survival and DNA synthesis, and is induced by sustained activation of ERK1/2. [62][63][64][65][66] Our data suggest that RAGE signaling in TE671/RAGE cells might down-regulate the expression of cyclin D1 via p38 MAPK-dependent inhibition of ERK1/2 and JNK activities. 28,67 After the submission of the present work, data have appeared showing that p38 MAPK causes myoblast proliferation arrest by inactivating JNK via up-regulation of MAPK phosphatase-1.…”

Section: Discussionmentioning

confidence: 91%

RAGE Expression in Rhabdomyosarcoma Cells Results in Myogenic Differentiation and Reduced Proliferation, Migration, Invasiveness, and Tumor Growth

Riuzzi

Sorci

Donato

2007

The American Journal of Pathology

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Activation of receptor for advanced glycation end products (RAGE) by its ligand, HMGB1, stimulates myogenesis via a Cdc42-Rac1-MKK6-p38 mitogen-activated protein kinase pathway. In addition, functional inactivation of RAGE in myoblasts results in reduced myogenesis, increased proliferation, and tumor formation in vivo. We show here that TE671 rhabdomyosarcoma cells, which do not express RAGE, can be induced to differentiate on transfection with RAGE (TE671/RAGE cells) but not a signalingdeficient RAGE mutant (RAGE⌬cyto) (TE671/ RAGE⌬cyto cells) via activation of a Cdc42-Rac1-MKK6-p38 pathway and that TE671/RAGE cell differentiation depends on RAGE engagement by HMGB1. TE671/RAGE cells also show p38-dependent inactivation of extracellular signal-regulated kinases 1 and 2 and c-Jun NH 2 terminal protein kinase and reduced proliferation, migration, and invasiveness and increased apoptosis, volume, and adhesiveness in vitro; they also grow smaller tumors and show a lower tumor incidence in vivo compared with wildtype cells. Two other rhabdomyosarcoma cell lines that express RAGE, CCA and RMZ-RC2, show an inverse relationship between the level of RAGE expression and invasiveness in vitro and exhibit reduced myogenic potential and enhanced invasive properties in vitro when transfected with RAGE⌬cyto. The rhabdomyosarcoma cell lines used here and C2C12 myoblasts express and release HMGB1, which activates RAGE in an autocrine manner. These data suggest that deregulation of RAGE expression in myoblasts might concur in rhabdomyosarcomagenesis and that increasing RAGE expression in

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“…Reduction of EWS/FLI-1 expression decreases EFT cell growth in vitro and tumor-forming capacity in vivo, showing that these oncoproteins maintain cellular proliferation and survival (Tanaka et al, 1997;Prieur et al, 2004;Hu-Lieskovan et al, 2005a). Accordingly EWS/ETS proteins regulate expression from the proliferation-associated MYC, CCND1, TGFBR2, CDKN1A and p57KIP genes (Bailly et al, 1994;Hahm et al, 1999;Dauphinot et al, 2001;Nakatani et al, 2003;Zhang et al, 2004). EWS/ETS proteins also regulate differentiation of a variety of cell types (Eliazer et al, 2003;Torchia et al, 2003;Rorie et al, 2004;Riggi et al, 2005;Hu-Lieskovan et al, 2005b;Yeny et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

EWS/ETS proteins promote expression and regulate function of the homeodomain transcription factor BRN3A

et al. 2010

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Ewing's sarcoma family tumors (ESFTs or EFTs) express neuronal markers, which indicates they may originate from cells at least partly committed to neuronal lineage. However, recent publications suggest EFT originates in mesenchymal stem cells, and EWS/ETS fusion proteins characteristic of EFT activate neuronal marker expression to confer a neural phenotype on EFT. Here we show that the neuronal marker BRN3A/POU4F1 is expressed abundantly at the protein level in primary EFT but not in rhabdomyosarcoma and neuroblastoma, and EFT cells exhibit high activity of the BRN3A proximal autoregulatory region. EWS/FLI-1 siRNA reduces BRN3A expression and promoter activity and EWS/ETS proteins are bound to the BRN3A locus, suggesting a direct function for EWS/ETS proteins in control of BRN3A expression. Differentiation-associated and autoregulatory activities of BRN3A are respectively impaired and altered in EFT cells, and EWS/FLI-1 siRNA can restore some BRN3A function. A potentially novel function for BRN3A in EFT cells is identified. These results extend the hypothesis that EWS/ETS proteins induce expression of neuronal markers such as BRN3A in EFT by showing that the function of those same markers may be restricted or controlled in an EWS/ETS-dependent manner.

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Selective Usage of D-Type Cyclins by Ewing’s Tumors and Rhabdomyosarcomas

Cited by 57 publications

References 55 publications

Inhibition of Platelet-derived Growth Factor-induced Cell Growth Signaling by a Short Interfering RNA for EWS-Fli1 via Down-regulation of Phospholipase D2 in Ewing Sarcoma Cells

Inhibition of Platelet-derived Growth Factor-induced Cell Growth Signaling by a Short Interfering RNA for EWS-Fli1 via Down-regulation of Phospholipase D2 in Ewing Sarcoma Cells

RAGE Expression in Rhabdomyosarcoma Cells Results in Myogenic Differentiation and Reduced Proliferation, Migration, Invasiveness, and Tumor Growth

EWS/ETS proteins promote expression and regulate function of the homeodomain transcription factor BRN3A

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