RNA splicing mediated by YB‐1 is inhibited by TLS/CHOP in human myxoid liposarcoma cells

Rapp, Timothy; Yang, Liu; Conrad, Ernest U.; Mandahl, Nils; Chansky, Howard A.

doi:10.1016/s0736-0266(02)00006-2

Cited by 29 publications

(18 citation statements)

References 33 publications

(12 reference statements)

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“…Seven proteins among 20 bands were identified, and these were YB‐1, DDX1, phenylalaninyl‐tRNA synthetase α and β subunits, amylo‐1,6‐glucosidase, and several small and large ribosomal subunits. YB‐1 is a multifunctional RNA/DNA binding protein and has a role in transcriptional and posttranscriptional RNA metabolism, including splicing (Stickeler et al, 2001; Rapp et al, 2002; Kohno et al, 2003; Raffetseder et al, 2003; Allemand et al, 2007). DDX1 is part of the DEAD box RNA helicase family (Cordin et al, 2006).…”

Section: Resultsmentioning

confidence: 99%

MBNL1 associates with YB‐1 in cytoplasmic stress granules

Onishi

Kino

Morita

et al. 2008

J of Neuroscience Research

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The muscleblind-like (MBNL) protein family is thought to be involved in the molecular mechanism of myotonic dystrophy (DM). Although it has been shown to have splicing activity, a broader function in cellular RNA metabolism has been implicated. In this study, we attempted to find the binding proteins of MBNL1 in order to elucidate its physiological function. First, we performed a GST pull-down assay using GST-MBNL1-6xHis as bait. Several proteins were identified, including YB-1, a multifunctional DNA/RNA-binding protein, and DDX1, a DEAD box RNA helicase. MBNL1 formed an RNP complex with YB-1 and DDX1 in binding assays. YB-1 also showed a weak but significant effect on alpha-actinin splice site selection. Interestingly, in response to stress, MBNL1 moved to cytoplasmic stress granules, where it colocalized with YB-1, which was previously reported to be a component of stress granules. We found that DDX1 also colocalized with MBNL1 at stress granules. These results provide new insight into the dynamics of MBNL1 in response to stress, and they suggest a role for MBNL1 in mRNA metabolism in the cytoplasm.

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Section: Resultsmentioning

confidence: 99%

MBNL1 associates with YB‐1 in cytoplasmic stress granules

Onishi

Kino

Morita

et al. 2008

J of Neuroscience Research

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“…In addition, by fusing the B-ZIP domain of CREB3L2 to the Nterminal part of FUS, the ability to dimerize with other members of the OASIS family could be affected (Barone et al, 1994;Zinszner et al, 1994Zinszner et al, , 1997. In addition, it is reasonable to assume that the FUS/CREB3L2 chimera would retain the ability, as do FUS/DDIT3 and FUS/ERG (Chansky et al, 2001;Rapp et al, 2002), to bind to RNA polymerase II via the N-terminal part of FUS but would lack the ability to recruit the transcription and translation factor Y-box binding protein-1 (YB-1) because of the replacement of the central and C-terminal parts of FUS by CREB3L2. Consequently, RNA splicing mediated by YB-1 also would be expected to be inhibited.…”

Section: Discussionmentioning

confidence: 99%

The chimeric FUS/CREB3l2 gene is specific for low‐grade fibromyxoid sarcoma

Panagopoulos

Storlazzi

Fletcher

et al. 2004

Genes Chromosomes & Cancer

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196

147

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Low-grade fibromyxoid sarcoma (LGFMS) is a variant of fibrosarcoma that was recognized as a distinct tumor entity only quite recently. We previously described a translocation, t(7;16)(q33;p11), that resulted in a fusion of the FUS and CREB3L2 (also known as BBF2H7) genes in two soft tissue tumors that fulfilled morphologic criteria for LGFMS. To delineate the spectrum of tumors that may harbor the FUS/CREB3L2 gene, we selected 45 low-grade spindle cell sarcomas for reverse transcriptase polymerase chain reaction (RT-PCR) and/or fluorescence in situ hybridization (FISH) analyses; none of these tumors had originally been diagnosed as LGFMS. Furthermore, also included were two benign soft tissue tumors and nine high-grade sarcomas with supernumerary ring chromosomes or 7q3 rearrangement and three tumors diagnosed as LGFMS prior to the genetic analysis. Of the 59 tumors analyzed, 12 were FUS/CREB3L2-positive, all of which were diagnosed at histopathologic re-examination as being LGFMS, of both the classical subtype and the subtype with giant collagen rosettes. The breakpoints in the fusion transcripts were always in exons 6 or 7 of FUS and exon 5 of CREB3L2. The results indicated that FUS/CREB3L2 is specifically associated with LGFMS and that RT-PCR or FISH analysis may be useful for the differential diagnosis.

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“…This state of affairs exists for several reasons. The molecular pathogenesis of EFTs appears to be very complex with disruptions of both gene transcription and pre-mRNA splicing [6,18,19,34,43] leading to a potentially wide array of secondary downstream changes in gene expression. Perhaps even more critical has been the difficulty in isolating the effects of the EWS/FLI-I chimeric fusion protein in Ewing's tumor cells.…”

Section: Discussionmentioning

confidence: 99%

Targeting of EWS/FLI‐1 by RNA interference attenuates the tumor phenotype of Ewing's sarcoma cells in vitro

Chansky

Barahmand‐pour

Mei

et al. 2004

Journal Orthopaedic Research

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The dcfining cytogenetic abnormality of Ewing's sarcoma is the presence of a balanced t( 1 1;22) translocation expressing the EWSIFLI-I chimeric fusion protein. The effect of EWSIFLI-1 appears to be dominant negative since over-expression of EWS does not overcome the sarcoma phenotype. Previous studies have shown that EWSIFLI-1 as well as related sarcoma fusion proteins are necessary and sufficient to induce transformation both in vitro and in vivo. In this study we report that synthetic small interfering RNA (siRNA) specifically suppresses EWSIFLI-1 fusion gene expression in SK-ES Ewing's sarcoma cells. Knockdown of the EWSI FLI-1 fusion protein is correlated with decreased cell proliferation and increased apoptosis. We demonstrate that Ewing's sarcoma tumors as well as Ewing's sarcoma cell lines predominantly express the CXCR4 chemokine receptor. Using an in vitro invasion assay, the SDF-1 ligand of CXCR4 was shown to be a potent stimulus of invasion by SK-ES cells. Knockdown of EWSIFLI-1 by RNA interference abrogates the invasiveness of SK-ES cells. These experiments suggest that targeted silencing of the EWSIFLI-I fusion gene. by siRNA represents a promising strategy to study the loss of EWSIFLI-I protein in Ewing's sarcoma cells of otherwise identical genetic background.

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RNA splicing mediated by YB‐1 is inhibited by TLS/CHOP in human myxoid liposarcoma cells

Cited by 29 publications

References 33 publications

MBNL1 associates with YB‐1 in cytoplasmic stress granules

MBNL1 associates with YB‐1 in cytoplasmic stress granules

The chimeric FUS/CREB3l2 gene is specific for low‐grade fibromyxoid sarcoma

Targeting of EWS/FLI‐1 by RNA interference attenuates the tumor phenotype of Ewing's sarcoma cells in vitro

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