Premium
Calreticulin up‐regulates VEGF‐A and VEGF‐C in SK‐N‐DZ and SH‐SY5Y neuroblastoma cell lines
Author(s) -
Lin Kuan-Hung,
Wu Pei-Yi,
Lee Hsinyu
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.657.5
Subject(s) - calreticulin , neuroblastoma , angiogenesis , cancer research , metastasis , carcinogenesis , sh sy5y , vascular endothelial growth factor , downregulation and upregulation , endoplasmic reticulum , biology , chemistry , cancer , medicine , microbiology and biotechnology , cell culture , vegf receptors , biochemistry , gene , genetics
Neuroblastoma is a childhood cancer with low survival rate and great potential of metastasis. Even though there are several clinically relevant prognostic markers have been identified, the molecular mechanism underlying the tumorigenesis of NB is still unknown. Calreticulin (CRT), an endoplasmic reticulum chaperone protein, is one of the biomarker of neuroblastoma. It was suggested to play a critical role in the tumorigenesis and differentiation in neuroblastoma. In gastric cancer cells, it was also found that CRT strongly enhances angiogenesis by promoting the expression of vascular endothelial growth factors (VEGFs). In this study, we aim to investigate the correlation between CRT and VEGF‐A and VEGF‐C in neuroblastoma. Overexpression of CRT in SK‐N‐DZ and SH‐SY5Y cells upregulates VEGF‐A and VEGF‐C expression at both mRNA and protein level. Furthermore, CRT siRNA efficiently suppresses CRT expression resulted in downregulation of VEGF‐A and VEGF‐C. These results indicate that CRT plays a role in regulating VEGFs expression, which may affect angiogenesis and lymphangiogenesis in neuroblastoma. However, the underlying mechanism of how CRT regulating neuroblastoma metastasis still remain to be clarified.