Carcinogenesis Advance Access originally published online on July 5, 2007
Carcinogenesis 2007 28(10):2122-2130; 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, NJ, 08540 USA
3 Department of Paediatric Surgery, The Second Affiliated Hospital of China Medical University, Shenyang, 110004 China
4 Department of Paediatric Surgery, Beijing Children's Hospital, Capital University of Medical Sciences, Beijing, 100045 China
5 Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ, 08854 USA
* To whom correspondence should be addressed. Tel: +732 445 2061; Fax: +732 445 2063; Email: ren{at}dls.rutgers.edu
Correspondence may also be addressed to Paul K.H. Tam. Tel: +852 2855 4580; Fax: +852 2817 3155; Email: 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 that were carried out by proliferative and invasive phenotypes of tumor cells, respectively. Two subpopulations from human neuroblastoma cell line were isolated: highly invasive (HI) cells and low-invasive (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 reverse transcriptase–polymerase chain reaction revealed that visinin-like protein-1 (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 with 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. Up-regulation of VSNL-1 potentiated the anoikis-resistant ability of neuroblastoma cell. The expression of anoikis inhibitor TrkB, intracellular adhesion molecule 1, major histocompatibility complex class I, 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.
Abbreviations: DMEM, Dulbecco's modified Eagle's medium; ERK, extracellular signal-related kinase; FBS, fetal bovine serum; FITC, fluorescein isothiocyanate; FACS, fluorescence-activated cell sorting; HI, highly invasive; ICAM-1, intracellular adhesion molecule 1; i.v, intravenously; LI, low invasive; MHC-I, major histocompatibility complex class I; PBS, phosphate-buffered saline; p-Akt, phosphorylated-Akt; PI, propidium iodide; qRT–PCR, quantitative reverse transcriptase–polymerase chain reaction; s.c, subcutaneously; VSNL-1, visinin-like protein-1
Received January 5, 2007; revised June 3, 2007; accepted June 24, 2007.
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