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Neurocan, an extracellular chondroitin sulfate proteoglycan, stimulates neuroblastoma cells to promote malignant phenotypes.
Su, Zhendong; Kishida, Satoshi; Tsubota, Shoma; Sakamoto, Kazuma; Cao, Dongliang; Kiyonari, Shinichi; Ohira, Miki; Kamijo, Takehiko; Narita, Atsushi; Xu, Yinyan; Takahashi, Yoshiyuki; Kadomatsu, Kenji.
Afiliación
  • Su Z; Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
  • Kishida S; Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
  • Tsubota S; Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
  • Sakamoto K; Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
  • Cao D; Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
  • Kiyonari S; Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
  • Ohira M; Research Institute for Clinical Oncology, Saitama Cancer Center, Saitama, Saitama, Japan.
  • Kamijo T; Research Institute for Clinical Oncology, Saitama Cancer Center, Saitama, Saitama, Japan.
  • Narita A; Department of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
  • Xu Y; Department of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
  • Takahashi Y; Department of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
  • Kadomatsu K; Department of Biochemistry, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Oncotarget ; 8(63): 106296-106310, 2017 Dec 05.
Article en En | MEDLINE | ID: mdl-29290949
Neurocan (NCAN), a secreted chondroitin sulfate proteoglycan, is one of the major inhibitory molecules for axon regeneration in nervous injury. However, its role in cancer is not clear. Here we observed that high NCAN expression was closely associated with the unfavorable outcome of neuroblastoma (NB). NCAN was also highly and ubiquitously expressed in the early lesions and terminal tumor of TH-MYCN mice, a NB model. Interestingly, exogenous NCAN (i.e., overexpression, recombinant protein and conditioned medium) transformed adherent NB cells into spheres whose malignancies in vitro (anchorage-independent growth and chemoresistance) and in vivo (xenograft tumor growth) were potentiated. Both chondroitin sulfate sugar chains and NCAN's core protein were essential for the sphere formation. The CSG3 domain was essential in the moiety of NCAN. Our comprehensive microarray analysis and RT-qPCR of mRNA expression suggested that NCAN treatment promoted cell division, and urged cells to undifferentiated state. The knockdown of NCAN in tumor sphere cells cultured from TH-MYCN mice resulted in growth suppression in vitro and in vivo. Our findings suggest that NCAN, which stimulates NB cells to promote malignant phenotypes, is an extracellular molecule providing a growth advantage to cancer cells.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: Oncotarget Año: 2017 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: Oncotarget Año: 2017 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos