☆ 4.3 Article

MIF, secreted by human hepatic sinusoidal endothelial cells, promotes chemotaxis and outgrowth of colorectal cancer in liver prometastasis

ONCOTARGET (2015)

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期刊

ONCOTARGET
卷 6, 期 26, 页码 22410-22423

出版社

IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.4198

关键词

colorectal cancer; hepatic sinusoidal endothelial cell; macrophage migration inhibitory factor; chemotaxis; metastasis

类别

Oncology Cell Biology

资金

  1. National Basic Research Program of China (973 program) [2015CB554002, 2010CB529403]
  2. National Natural Science Foundation of China - NSFC-Guangdong Joint Fund [U1201226]
  3. National Natural Science Foundation of China [81090422, 81172381, 81372584, 81472313, 81071735]
  4. Guangdong Provincial Natural Science Foundation of China [S2012010009643]
  5. Science and Technology Innovation Foundation of Guangdong Higher Education [CXZD1016]
  6. National Natural Science Foundation of Guangdong [2010B031500012]
  7. Guangzhou Science & Technology Plan Project [201300000056]

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Growth and invasion of metastatic colorectal cancer (CRC) cells in the liver depend on microenvironment. Here, we showed that human hepatic sinusoidal endothelial cells (HHSECs) induce chemotaxis and outgrowth of CRC cells. Macrophage migration inhibitory factor (MIF), released by HHSECs, stimulated chemotaxis of CRC cells. MIF secreted by HHSECs, but not by CRC cells themselves, promoted migration and epithelial-mesenchymal transition (EMT) and facilitated proliferation and apoptotic resistance of CRC cells. In orthotopic implantation models in nude mice, exogenous MIF stimulated growth of CRC cells and metastasis. Furthermore, MIF accelerated mobility of CRC cells by suppressing F-actin depolymerization and phosphorylating cofilin. Noteworthy, MIF levels were correlated with the size of hepatic metastases. We suggest that HHSECs and paracrine MIF promote initial migration and proliferation of CRC cells in the hepatic sinusoids to generate liver metastases.

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