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RNA helicase A activity is inhibited by oncogenic transcription factor EWS-FLI1

Erkizan, Hayriye Verda ; Schneider, Jeffrey A. ; Sajwan, Kamal ; [et al.]

Oxford University Press (OUP) ; 2015

In: Nucleic Acids Research Vol. 43, No. 2 ( 2015-01-30), p. 1069-1080

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In: Nucleic Acids Research, Oxford University Press (OUP), Vol. 43, No. 2 ( 2015-01-30), p. 1069-1080

Type of Medium: Online Resource

ISSN: 1362-4962 , 0305-1048

URL: Article

DOI: 10.1093/nar/gku1328

RVK:

WA 15000

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2015

detail.hit.zdb_id: 1472175-2

SSG: 12

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Oncoprotein EWS-FLI1 Activity Is Enhanced by RNA Helicase A

Toretsky, Jeffrey A. ; Erkizan, Verda ; Levenson, Amy ; [et al.]

American Association for Cancer Research (AACR) ; 2006

In: Cancer Research Vol. 66, No. 11 ( 2006-06-01), p. 5574-5581

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In: Cancer Research, American Association for Cancer Research (AACR), Vol. 66, No. 11 ( 2006-06-01), p. 5574-5581

Abstract: RNA helicase A (RHA), a member of the DEXH box helicase family of proteins, is an integral component of protein complexes that regulate transcription and splicing. The EWS-FLI1 oncoprotein is expressed as a result of the chromosomal translocation t(11;22) that occurs in patients with the Ewing's sarcoma family of tumors (ESFT). Using phage display library screening, we identified an EWS-FLI1 binding peptide containing homology to RHA. ESFT cell lines and patient tumors highly expressed RHA. GST pull-down and ELISA assays showed that EWS-FLI1 specifically bound RHA fragment amino acids 630 to 1020, which contains the peptide region discovered by phage display. Endogenous RHA was identified in a protein complex with EWS-FLI1 in ESFT cell lines. Chromatin immunoprecipitation experiments showed both EWS-FLI1 and RHA bound to EWS-FLI1 target gene promoters. RHA stimulated the transcriptional activity of EWS-FLI1 regulated promoters, including Id2, in ESFT cells. In addition, RHA expression in mouse embryonic fibroblast cells stably transfected with EWS-FLI1 enhanced the anchorage-independent phenotype above that with EWS-FLI1 alone. These results suggest that RHA interacts with EWS-FLI1 as a transcriptional cofactor to enhance its function. (Cancer Res 2006; 66(11): 5574-81)

Type of Medium: Online Resource

ISSN: 0008-5472 , 1538-7445

URL: Article

DOI: 10.1158/0008-5472.CAN-05-3293

RVK:

XA 36000

RVK:

XA 10000

Language: English

Publisher: American Association for Cancer Research (AACR)

Publication Date: 2006

detail.hit.zdb_id: 2036785-5

detail.hit.zdb_id: 1432-1

detail.hit.zdb_id: 410466-3

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Tumor Expression of 4-1BB Ligand Sustains Tumor Lytic T Cells

Zhang, Hua ; Merchant, Melinda S. ; Chua, Kevin S. ; [et al.]

Informa UK Limited ; 2003

In: Cancer Biology & Therapy Vol. 2, No. 5 ( 2003-09-04), p. 579-586

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In: Cancer Biology & Therapy, Informa UK Limited, Vol. 2, No. 5 ( 2003-09-04), p. 579-586

Type of Medium: Online Resource

ISSN: 1538-4047 , 1555-8576

URL: Article

DOI: 10.4161/cbt.2.5.545

Language: English

Publisher: Informa UK Limited

Publication Date: 2003

detail.hit.zdb_id: 2088895-8

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Clofarabine induces ERK/MSK/CREB activation through inhibiting CD99 on Ewing sarcoma cells

Sevim, Handan ; Çelik, Haydar ; Düşünceli, Levent ; [et al.]

Public Library of Science (PLoS) ; 2021

In: PLOS ONE Vol. 16, No. 6 ( 2021-6-16), p. e0253170-

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In: PLOS ONE, Public Library of Science (PLoS), Vol. 16, No. 6 ( 2021-6-16), p. e0253170-

Abstract: Clofarabine, an FDA approved purine analog, is used in the treatment of relapsed or refractory acute lymphoblastic leukemia. Clofarabine acts by inhibiting DNA synthesis. We demonstrated that clofarabine may have a novel function though inhibiting CD99, a transmembrane protein highly expressed on Ewing Sarcoma (ES) cells. CD99 is a validated target in ES whose inhibition may lead to a high therapeutic index for patients. Here we present additional data to support the hypothesis that clofarabine acts on CD99 and regulates key signaling pathways in ES. Cellular thermal shift assay indicated a direct interaction between clofarabine and CD99 in ES cell lysates. Clofarabine induced ES cell death does not require clofarabine’s conversion to its active form by deoxycytidine kinase. A phosphokinase array screen with clofarabine and a CD99 blocking antibody identified alterations in signaling pathways. CD99 inhibition with clofarabine in ES cells caused rapid and sustained phosphorylation of ERK, MSK, and CREB. However, activation of this pathway did not correlate with clofarabine induced ES cell death. In summary, we demonstrated that clofarabine may activate ERK, MSK, and CREB phosphorylation through CD99 within minutes, however this paradoxical activation and subsequent ES cell death requires additional investigation.

Type of Medium: Online Resource

ISSN: 1932-6203

URL: Article

DOI: 10.1371/journal.pone.0253170

DOI: 10.1371/journal.pone.0253170.g001

DOI: 10.1371/journal.pone.0253170.g002

DOI: 10.1371/journal.pone.0253170.g003

DOI: 10.1371/journal.pone.0253170.g004

DOI: 10.1371/journal.pone.0253170.g005

DOI: 10.1371/journal.pone.0253170.s001

DOI: 10.1371/journal.pone.0253170.s002

DOI: 10.1371/journal.pone.0253170.s003

DOI: 10.1371/journal.pone.0253170.s004

DOI: 10.1371/journal.pone.0253170.s005

DOI: 10.1371/journal.pone.0253170.s006

DOI: 10.1371/journal.pone.0253170.s007

Language: English

Publisher: Public Library of Science (PLoS)

Publication Date: 2021

detail.hit.zdb_id: 2267670-3

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Wnt/Frizzled signaling in Ewing sarcoma : Wnt Signaling in ESFT

Üren, Aykut ; Wolf, Vladimir ; Sun, Yu-Feng ; [et al.]

Wiley ; 2004

In: Pediatric Blood & Cancer Vol. 43, No. 3 ( 2004-09), p. 243-249

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In: Pediatric Blood & Cancer, Wiley, Vol. 43, No. 3 ( 2004-09), p. 243-249

Type of Medium: Online Resource

ISSN: 1545-5009

URL: Issue

URL: Article

DOI: 10.1002/pbc.v43:3

DOI: 10.1002/pbc.20124

Language: English

Publisher: Wiley

Publication Date: 2004

detail.hit.zdb_id: 2130978-4

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Wnt-3a and Dickkopf-1 Stimulate Neurite Outgrowth in Ewing Tumor Cells via a Frizzled3- and c-Jun N-Terminal Kinase-Dependent Mechanism

Endo, Yoshimi ; Beauchamp, Elspeth ; Woods, David ; [et al.]

Informa UK Limited ; 2008

In: Molecular and Cellular Biology Vol. 28, No. 7 ( 2008-04-01), p. 2368-2379

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In: Molecular and Cellular Biology, Informa UK Limited, Vol. 28, No. 7 ( 2008-04-01), p. 2368-2379

Type of Medium: Online Resource

ISSN: 1098-5549

URL: Article

DOI: 10.1128/MCB.01780-07

Language: English

Publisher: Informa UK Limited

Publication Date: 2008

detail.hit.zdb_id: 1474919-1

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The genomic landscape of juvenile myelomonocytic leukemia

Stieglitz, Elliot ; Taylor-Weiner, Amaro N ; Chang, Tiffany Y ; [et al.]

Springer Science and Business Media LLC ; 2015

In: Nature Genetics Vol. 47, No. 11 ( 2015-11), p. 1326-1333

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In: Nature Genetics, Springer Science and Business Media LLC, Vol. 47, No. 11 ( 2015-11), p. 1326-1333

Type of Medium: Online Resource

ISSN: 1061-4036 , 1546-1718

URL: Article

DOI: 10.1038/ng.3400

RVK:

XA 10000

Language: English

Publisher: Springer Science and Business Media LLC

Publication Date: 2015

detail.hit.zdb_id: 1494946-5

SSG: 12

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Correction: Corrigendum: The genomic landscape of juvenile myelomonocytic leukemia

Stieglitz, Elliot ; Taylor-Weiner, Amaro N ; Chang, Tiffany Y ; [et al.]

Springer Science and Business Media LLC ; 2016

In: Nature Genetics Vol. 48, No. 1 ( 2016-1), p. 101-101

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In: Nature Genetics, Springer Science and Business Media LLC, Vol. 48, No. 1 ( 2016-1), p. 101-101

Type of Medium: Online Resource

ISSN: 1061-4036 , 1546-1718

URL: Article

DOI: 10.1038/ng0116-101a

RVK:

XA 10000

Language: English

Publisher: Springer Science and Business Media LLC

Publication Date: 2016

detail.hit.zdb_id: 1494946-5

SSG: 12

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Mutational Inactivation of STAG2 Causes Aneuploidy in Human Cancer

Solomon, David A. ; Kim, Taeyeon ; Diaz-Martinez, Laura A. ; [et al.]

American Association for the Advancement of Science (AAAS) ; 2011

In: Science Vol. 333, No. 6045 ( 2011-08-19), p. 1039-1043

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In: Science, American Association for the Advancement of Science (AAAS), Vol. 333, No. 6045 ( 2011-08-19), p. 1039-1043

Abstract: Most cancer cells are characterized by aneuploidy, an abnormal number of chromosomes. We have identified a clue to the mechanistic origins of aneuploidy through integrative genomic analyses of human tumors. A diverse range of tumor types were found to harbor deletions or inactivating mutations of STAG2 , a gene encoding a subunit of the cohesin complex, which regulates the separation of sister chromatids during cell division. Because STAG2 is on the X chromosome, its inactivation requires only a single mutational event. Studying a near-diploid human cell line with a stable karyotype, we found that targeted inactivation of STAG2 led to chromatid cohesion defects and aneuploidy, whereas in two aneuploid human glioblastoma cell lines, targeted correction of the endogenous mutant alleles of STAG2 led to enhanced chromosomal stability. Thus, genetic disruption of cohesin is a cause of aneuploidy in human cancer.

Type of Medium: Online Resource

ISSN: 0036-8075 , 1095-9203

URL: Article

DOI: 10.1126/science.1203619

RVK:

TA 1000

RVK:

WA 15000

Language: English

Publisher: American Association for the Advancement of Science (AAAS)

Publication Date: 2011

detail.hit.zdb_id: 128410-1

detail.hit.zdb_id: 2066996-3

detail.hit.zdb_id: 2060783-0

SSG: 11

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Midline Carcinoma of Children and Young Adults With NUT Rearrangement

French, Christopher A. ; Kutok, Jeffery L. ; Faquin, William C. ; [et al.]

American Society of Clinical Oncology (ASCO) ; 2004

In: Journal of Clinical Oncology Vol. 22, No. 20 ( 2004-10-15), p. 4135-4139

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In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 22, No. 20 ( 2004-10-15), p. 4135-4139

Abstract: A balanced chromosomal translocation, t(15;19), resulting in the BRD4-NUT oncogene, has been identified in a lethal carcinoma of young people, a disease described primarily in case reports. We sought to amass a more definitive series of tumors with NUT and/or BRD4 gene rearrangements and to determine distinct clinicopathologic features. Patients and Methods Carcinomas (N = 98) in young individuals (median age, 32.5 years) were screened for NUT and BRD4 rearrangements using dual-color fluorescence in situ hybridization. Four published carcinomas with BRD4 and NUT rearrangements were also evaluated. Immunophenotypic analyses were performed. Results Eleven tumors had NUT gene rearrangements, including eight with BRD4-NUT fusions and three with novel rearrangements, which were designated as NUT variant. All NUT-rearranged carcinomas (NRCs) arose from midline epithelial structures, including the first example arising below the diaphragm. Patients were young (median age, 17.6 years). Squamous differentiation (seen in 82% of NRCs) was particularly striking in NUT-variant cases. In this first description of NUT-variant carcinomas, the average survival (96 weeks, n = 3) was longer than for BRD4-NUT carcinomas (28 weeks, n = 8). Strong CD34 expression was found in six of 11 NRCs but in zero of 45 NUT wild-type carcinomas. Conclusion NRCs arise from midline structures in young people, and NRCs with BRD4-NUT are highly lethal, despite intensive therapies. NUT-variant carcinomas might have a less fulminant clinical course than those with BRD4-NUT fusions. CD34 expression is characteristic in NRCs and, therefore, holds promise as a diagnostic test for this distinctive clinicopathologic entity.

Type of Medium: Online Resource

ISSN: 0732-183X , 1527-7755

URL: Article

DOI: 10.1200/JCO.2004.02.107

RVK:

XA 52760

RVK:

XA 10000

Language: English

Publisher: American Society of Clinical Oncology (ASCO)

Publication Date: 2004

detail.hit.zdb_id: 2005181-5

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