MYCN transcriptionally represses CD9 to trigger an invasion-metastasis cascade in neuroblastoma

نویسندگان

  • Johannes Fabian
  • Desirée Opitz
  • Kristina Althoff
  • Marco Lodrini
  • Kathy Astrahantseff
  • Barbara Hero
  • Ruth Volland
  • Anneleen Beckers
  • Katleen de Preter
  • Nitin S Patil
  • Mohammed L Abba
  • Theresa M Thole
  • Jasmin Wünschel
  • Annette Künkele
  • Jamie Hu
  • Leonille Schweizer
  • Gunhild Mechtersheimer
  • Daniel R Carter
  • Belamy B Cheung
  • Odilia Popanda
  • Andreas von Deimling
  • Kai-Oliver Henrich
  • Frank Westermann
  • Manfred Schwab
  • Jan Koster
  • Rogier Versteeg
  • Glenn M Marshall
  • Frank Speleman
  • Margot Zoeller
  • Heike Allgayer
  • Matthias Fischer
  • Frank Berthold
  • Andreas E Kulozik
  • Olaf Witt
  • Angelika Eggert
  • Johannes H Schulte
  • Hedwig E Deubzer
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MYCN and HDAC5 transcriptionally repress CD9 to trigger invasion and metastasis in neuroblastoma

The systemic and resistant nature of metastatic neuroblastoma renders it largely incurable with current multimodal treatment. Clinical progression stems mainly from the increasing burden of metastatic colonization. Therapeutically inhibiting the migration-invasion-metastasis cascade would be of great benefit, but the mechanisms driving this cycle are as yet poorly understood. In-depth transcrip...

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Combined IFN-; and retinoic acid treatment targets the N-Myc/Max/Mad1 network resulting in repression of N-Myc target genes in MYCN-amplified neuroblastoma cells

The MYCN protooncogene is involved in the control of cell proliferation, differentiation, and survival of neuroblasts. Deregulation of MYCN by gene amplification contributes to neuroblastoma development and is strongly correlated to advanced disease and poor outcome, emphasizing the urge for new therapeutic strategies targeting MYCN function. The transcription factor N-Myc, encoded by MYCN, reg...

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Galectin-3 Impairment of MYCN-Dependent Apoptosis-Sensitive Phenotype Is Antagonized by Nutlin-3 in Neuroblastoma Cells

MYCN amplification occurs in about 20-25% of human neuroblastomas and characterizes the majority of the high-risk cases, which display less than 50% prolonged survival rate despite intense multimodal treatment. Somehow paradoxically, MYCN also sensitizes neuroblastoma cells to apoptosis, understanding the molecular mechanisms of which might be relevant for the therapy of MYCN amplified neurobla...

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Rho-associated kinase is a therapeutic target in neuroblastoma.

Neuroblastoma is a peripheral neural system tumor that originates from the neural crest and is the most common and deadly tumor of infancy. Here we show that neuroblastoma harbors frequent mutations of genes controlling the Rac/Rho signaling cascade important for proper migration and differentiation of neural crest cells during neuritogenesis. RhoA is activated in tumors from neuroblastoma pati...

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Inactivation of SMC2 shows a synergistic lethal response in MYCN-amplified neuroblastoma cells

The condensin complex is required for chromosome condensation during mitosis; however, the role of this complex during interphase is unclear. Neuroblastoma is the most common extracranial solid tumor of childhood, and it is often lethal. In human neuroblastoma, MYCN gene amplification is correlated with poor prognosis. This study demonstrates that the gene encoding the condensin complex subunit...

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عنوان ژورنال:

دوره 2  شماره 

صفحات  -

تاریخ انتشار 2015