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Calreticulin‐Knockdown Suppresses Cell Proliferation, Migration and Adhesion in Human Bladder Cancer Cells
Author(s) -
Lu YiChien,
Chang ChengChi,
Lee Hsinyu
Publication year - 2009
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.23.1_supplement.740.17
Subject(s) - calreticulin , gene knockdown , transfection , cancer research , bladder cancer , small hairpin rna , microbiology and biotechnology , rna interference , cell migration , vascular endothelial growth factor , urothelial cell , cell growth , cell adhesion , chemistry , endoplasmic reticulum , biology , cell , cancer , cell culture , rna , vegf receptors , gene , biochemistry , genetics
Bladder cancer is a common urothelial cancer. Through proteomic approaches, calreticulin (CRT) has been identified as a urinary marker for bladder cancer. Calreticulin is a multifunctional Ca2+‐binding molecular chaperone in endoplasmic reticulum (ER) and regulates various cellular functions such as Ca2+ homeostasis, gene expression, and cell adhesion. In the present study, J82 bladder cancer cells stably transfected with RNAi of CRT were generated (J82 CRT‐RNAi) to investigate the physiological effects of CRT in bladder tumor. The results showed that knockdown of CRT expression suppressed cell proliferation, migration and adhesion. We further demonstrated that the mRNA expression and protein secretion levels of vascular endothelial growth factor‐A (VEGF‐A), an important angiogenic factor, were also decreased in these cells. In addition, we also observed that compared to control vector transfected cells, tumors derived from J82 CRT‐RNAi cells were significantly smaller in nude mice. These results suggested that CRT may play an important role in bladder tumor formation.