Differentiation of immature DCs into endothelial-like cells in human esophageal carcinoma tissue homogenates

Lu,Jing; Bai,Ruihua; Qin,Zhenzhu; Zhang,Yanyan; Zhang,Xiaoyan; Jiang,Yanan; Yang,Hongyan; Huang,Youtian; Li,Gang; Zhao,Mingyao; Dong,Ziming

doi:10.3892/or.2013.2491

Differentiation of immature DCs into endothelial-like cells in human esophageal carcinoma tissue homogenates

Authors:
- Jing Lu
- Ruihua Bai
- Zhenzhu Qin
- Yanyan Zhang
- Xiaoyan Zhang
- Yanan Jiang
- Hongyan Yang
- Youtian Huang
- Gang Li
- Mingyao Zhao
- Ziming Dong
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Affiliations: Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, P.R. China, Department of Pathology, Henan Tumor Hospital, Zhengzhou 450003, P.R. China, Department of Pathology, The First People's Hospital of Shangqiu, Shangqiu 476100, P.R. China, Department of Dermatology and Skin Science, Research Pavilion, Vancouver Coastal Health Research Institute, University of British Columbia, Vancouver, BC, Canada
Published online on: May 23, 2013 https://doi.org/10.3892/or.2013.2491
Pages: 739-744

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Abstract

We previously reported endothelial-like differentiation (ELD) of immature dendritic cells (iDCs) in the microenvironment derived from EC9706 human esophageal squamous cell carcinoma conditioned medium (CM). However, the CM is far different from the esophageal carcinoma tissue of patients. In addition, the potential role of peri-esophageal carcinoma in the ELD of iDCs is also unknown. In the present study, we showed that the tumor microenvironment derived from esophageal carcinoma homogenate promoted iDCs to differentiate from the DC pathway toward endothelial cells, while the peri-esophageal carcinoma homogenate did not have this function. During the course of ELD, ERK signaling pathway and CREB were activated. Blocking MEK, both the phosphorylation of ERK and CREB, and the ELD of iDCs were inhibited. These data suggest that esophageal carcinoma tissue, not peri-esophageal carcinoma tissue, can drive iDCs to differentiate into endothelial-like cells, instead of differentiation into mature DCs, thereby losing the ability of antigen presentation.

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