TY - JOUR
T1 - Phosphatase of regenerating liver-3 promotes motility and metastasis of mouse melanoma cells
AU - Wu, Xiaopeng
AU - Zeng, Hu
AU - Zhang, Xianming
AU - Zhao, Ying
AU - Sha, Haibo
AU - Ge, Xiaomei
AU - Zhang, Minyue
AU - Gao, Xiang
AU - Xu, Qiang
N1 - Funding Information:
Supported by the State Key Project Foundation of “the 10th 5-year plan” of China, the National Natural Science Foundation of China (no. 30300425 ), the Natural Science Foundation of Jiangsu Province (no. BK2003069 ), and the 973 program of China (no. 2002CB513000 ).
PY - 2004/6
Y1 - 2004/6
N2 - Recent reports suggested that phosphatase of regenerating liver (PRL)-3 might be involved in colorectal carcinoma metastasis with an unknown mechanism. Here we demonstrated that PRL-3 expression was up-regulated in human liver carcinoma compared with normal liver. PRL-3 was also highly expressed in metastatic melanoma B16-BL6 cells but not in its lowly metastatic parental cell line, B16 cells. B16 cells transfected with PRL-3 cDNA displayed morphological transformation from epithelial-like shape to fibroblast-like shape. PRL-3-overexpressed cells showed much higher migratory ability, which could be reversed by specific anti-sense oligodeoxynucleotide and the phosphatase inhibitors sodium orthovanadate or potassium bisperoxo oxovanadate V. Meanwhile, the expression of the catalytically inactive PRL-3 mutations (D72A or C104S) significantly reduced the cell migratory capability. In addition, PRL-3 transfectants demonstrated altered extracellular matrix adhesive property and up-regulated integrin-mediated cell spreading efficiency. Furthermore, we confirmed that PRL-3 could facilitate lung and liver metastasis of B16 cells in an experimental metastasis model in mice, consistent with accelerated proliferation and growth rate both in vitro and in vivo. Together, these observations provide convincing evidence that PRL-3 truly plays a causal role in tumor metastasis.
AB - Recent reports suggested that phosphatase of regenerating liver (PRL)-3 might be involved in colorectal carcinoma metastasis with an unknown mechanism. Here we demonstrated that PRL-3 expression was up-regulated in human liver carcinoma compared with normal liver. PRL-3 was also highly expressed in metastatic melanoma B16-BL6 cells but not in its lowly metastatic parental cell line, B16 cells. B16 cells transfected with PRL-3 cDNA displayed morphological transformation from epithelial-like shape to fibroblast-like shape. PRL-3-overexpressed cells showed much higher migratory ability, which could be reversed by specific anti-sense oligodeoxynucleotide and the phosphatase inhibitors sodium orthovanadate or potassium bisperoxo oxovanadate V. Meanwhile, the expression of the catalytically inactive PRL-3 mutations (D72A or C104S) significantly reduced the cell migratory capability. In addition, PRL-3 transfectants demonstrated altered extracellular matrix adhesive property and up-regulated integrin-mediated cell spreading efficiency. Furthermore, we confirmed that PRL-3 could facilitate lung and liver metastasis of B16 cells in an experimental metastasis model in mice, consistent with accelerated proliferation and growth rate both in vitro and in vivo. Together, these observations provide convincing evidence that PRL-3 truly plays a causal role in tumor metastasis.
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U2 - 10.1016/S0002-9440(10)63763-7
DO - 10.1016/S0002-9440(10)63763-7
M3 - Article
C2 - 15161639
AN - SCOPUS:2442655501
SN - 0002-9440
VL - 164
SP - 2039
EP - 2054
JO - American Journal of Pathology
JF - American Journal of Pathology
IS - 6
ER -