Carcinogenesis Advance Access published online on July 5, 2007
Carcinogenesis, doi:10.1093/carcin/bgm147
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Involvement of Visinin Like Protein-1 (VSNL-1) in Regulating Proliferative and Invasive Properties of Neuroblastoma
1 Department of Surgery, the University of Hong Kong, Hong Kong SAR, China
2 Statistics Laboratory, Princeton University, Princeton, New Jersey, USA
3 Department of Paediatric Surgery, the Second Affiliated Hospital of China Medical University, Shenyang, China
4 Department of Paediatric Surgery, Beijing Children's Hospital, Capital University of Medical Sciences, Beijing, China
5 Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, New Jersey, USA
* To whom correspondence should be addressed. Yi Ren, Phone: 732-445-2061; Fax: 732-445-2063; E-mail: ren{at}dls.rutgers.edu or Paul KH Tam, Phone: 852-2855-4580; Fax: 852-2817-3155; E-mail: paultam{at}hkucc.hku.hk.
Tumor growth and metastasis require that tumor cells must have either the potential to shift genetically or epigenetically between proliferative and invasive phenotypes or both phenotypes simultaneously. In the present study, we demonstrated that neuroblastoma growth and invasion were distinct processes which were carried out by proliferative and invasive phenotypes of tumor cells, respectively. Two sub-populations from human neuroblastoma cell line were isolated: highly-invasive cells (HI cells) and low-invasive cells (LI cells). HI and LI cells had different proliferative rate and metastatic ability in vitro and in vivo. In addition, they had distinct activated signal pathways and sensitivities to chemotherapy drugs. Affymetrix microarray and quantitative RT-PCR revealed that VSNL-1 mRNA in HI cells was significantly higher than that in LI cells. We also observed that VSNL-1 was over-expressed in tumor specimens from patients with distant organ metastases compared to those without metastases. Furthermore, the invasive and proliferative phenotypes of neuroblastoma cells could be exchanged by regulation of VSNL-1 expression in vitro and in vivo. Upregulation of VSNL-1 potentiated the anoikis-resistant ability of neuroblastoma cell. The expression of anoikis inhibitor TrkB, intracellular adhesion molecule 1 (ICAM-1), major histocompatibility complex class I (MHC-1), CD44 and CD44v6 was associated with VSNL-1 level. These results suggested that distinct roles of proliferative and invasive phenotypes contributed to neuroblastoma progression and strongly demonstrated that VSNL-1 played a very important role in neuroblastoma metastasis.
Received January 5, 2007; revised June 3, 2007; accepted June 24, 2007.
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