Brief description: Although fatty liver is associated with hepatocarcinogenesis, it is unclear whether fatty liver promotes hepatocellular carcinoma (HCC) progression. Through and in vivoimodels, we investigated whether steatotic liver promotes HCC progression and whether steatotic liver hepatic stellate cells (HSCs) are associated with HCC progression. Activated fatty liver HSCs significantly contributed to HCC proliferation and migration, and exhibited increased secretion of interleukin-α, vascular endothelial growth factor, and transforming growth factor-β in the tumor microenvironment.
Cancer Cell Biology
Fatty liver creates a pro-metastatic microenvironment for hepatocellular carcinoma through activation of hepatic stellate cells
Version of Record online: 4 AUG 2014
© 2014 UICC
International Journal of Cancer
Volume 136, Issue 4, pages E3–E13, 15 February, 2015
How to Cite
Mikuriya, Y., Tashiro, H., Kuroda, S., Nambu, J., Kobayashi, T., Amano, H., Tanaka, Y. and Ohdan, H. (2015), Fatty liver creates a pro-metastatic microenvironment for hepatocellular carcinoma through activation of hepatic stellate cells. Int. J. Cancer, 136: E3–E13. doi: 10.1002/ijc.29096
- Issue online: 10 DEC 2014
- Version of Record online: 4 AUG 2014
- Accepted manuscript online: 23 JUL 2014 03:41AM EST
- Manuscript Accepted: 10 JUL 2014
- Manuscript Received: 8 DEC 2013
- Ministry of Education, Culture, Sports, Science and Technology . Grant Number: 21591748
Additional Supporting Information may be found in the online version of this article.
|ijc29096-sup-0002-suppfig1.tif||20957K||Supporting Figure 1|
|ijc29096-sup-0003-suppfig2.tif||16719K||Supporting Figure 2|
|ijc29096-sup-0004-suppfig3.tif||6410K||Supporting Figure 3|
|ijc29096-sup-0005-suppfig4.tif||22441K||Supporting Figure 4|
|ijc29096-sup-0006-suppfig5.tif||10994K||Supporting Figure 5|
|ijc29096-sup-0007-suppfig6.tif||7428K||Supporting Figure 5|
Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.