Journal
EBIOMEDICINE
Volume 31, Issue -, Pages 287-298Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ebiom.2018.05.004
Keywords
ASPH; Hydroxylase; Hepatocellular carcinoma; Metastasis; Epithelial-mesenchymal transition; Vimentin
Funding
- State Key Project for Research of Infectious Diseases [2012ZX10002-016]
- 973 Program [2006CB806600]
- Creative Research Groups of National Natural Science Foundation of China [30921006]
- Shanghai Municipal Science and Technology [12431900803]
- National Natural Science Foundation of China [81301828]
- Shanghai Hospital Development Center [SHDC12015104]
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Over-expression of aspartyl (asparagynal)-beta-hydroxylase (ASPH) contributes to hepatocellular carcinoma (HCC) invasiveness, but the role of ASPH hydroxylase activity in this process remains to be defined. As such, the current study investigated the role of ASPH hydroxylase activity in downstream signalling of HCC tumorgenesis and, specifically, metastasis development. Over-expression of wild-type ASPH, but not a hydroxylase mutant, promoted HCC cell migration in vitro, as well as intrahepatic and distant metastases in vivo. The enhanced migration and epithelial to mesenchymal transition (EMT) activation was notably absent in response to hydroxylase activity blockade. Vimentin, a regulator of EMT, interacted with ASPH and likely mediated the effect of ASPH hydroxylase activity with cell migration. The enhanced hydroxylase activity in tumor tissues predicted worse prognoses of HCC patients. Collectively, the hydroxylase activity of ASPH affected HCC metastasis through interacting with vimentin and regulating EMT. As such, ASPH might be a promising therapeutic target of HCC. (C) 2018 Published by Elsevier B.V.
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