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

摘要: // Chun-Ting Hu 1, 2 , Li-Li Guo Na Feng Lei Zhang 3 Zhou 1 Ma Lan Shen Gui-Hui Tong Qian-Wen Yan Shi-Jie Zhu Xiu-Wu Bian 4 Mao-De Lai 5 Yong-Jian Deng Yan-Qing Ding Department of Pathology, Nanfang Hospital and School Basic Medical Sciences, Southern University, Guangzhou 510515, China Guangdong Provincial Key Laboratory Molecular Tumor General Surgery, Renji Hospital, Shanghai Jiaotong University Medicine, 200127, Southwest Third Military Chongqing 400038, Zhejiang Hangzhou 310006, Correspondence to: Deng, e-mail: dengyj@smu.edu.cn Ding, dyq@fimmu.com Keywords: colorectal cancer, hepatic sinusoidal endothelial cell, macrophage migration inhibitory factor, chemotaxis, metastasis Received: March 03, 2015      Accepted: May 20, Published: June 02, 2015 ABSTRACT Growth invasion metastatic cancer (CRC) cells in the liver depend on microenvironment. Here, we showed that human (HHSECs) induce chemotaxis outgrowth CRC cells. Macrophage factor (MIF), released by HHSECs, stimulated MIF secreted but not themselves, promoted epithelial-mesenchymal transition (EMT) facilitated proliferation apoptotic resistance In orthotopic implantation models nude mice, exogenous growth metastasis. Furthermore, accelerated mobility suppressing F-actin depolymerization phosphorylating cofilin. Noteworthy, levels were correlated with size metastases. We suggest HHSECs paracrine promote initial sinusoids to generate