Reham Helwa1,2,3, Anette Heller4, Stian Knappskog5,6, Andrea S Bauer7. 1. Molecular Cell Biology Lab, Zoology Department, Faculty of Science, Ain Shams University, Cairo, 11566, Egypt. reham.helwa@sci.asu.edu.eg. 2. Functional Genome Analysis, German Cancer Research Center (DKFZ), Heidelberg, Germany. reham.helwa@sci.asu.edu.eg. 3. Section of Oncology, Department of Clinical Science, University of Bergen, Bergen, Norway. reham.helwa@sci.asu.edu.eg. 4. Department of Surgery, Heidelberg University Hospital, Heidelberg, Germany. 5. Section of Oncology, Department of Clinical Science, University of Bergen, Bergen, Norway. 6. Department of Oncology, Haukeland University Hospital, Bergen, Norway. 7. Functional Genome Analysis, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Abstract
BACKGROUND: The ability of tumor cells to invade and metastasize is relevant to the process of cancer progression and, as such, it represents an obstacle to cancer cure. So far, limited information is available on interactions between circulating tumor cells and blood cells. It is well-documented that galectin-4 is upregulated in many types of tumor cells and is involved in metastasis. Here, we address the hypothesis that tumor cells may interact with red blood cells (RBCs) via galectin-4. METHODS: High galectin-4 expressing colon, normal pancreatic and pancreatic cancer-derived cell lines (n = 5) were incubated with peripheral blood cells from different donors. Their interactions and associated proteins were examined by immunostaining and live cell imaging. RESULTS: We found that (endogenous or exogenous) galectin-4 expressing tumor cells interact directly with RBCs. We also observed an accumulation of galectin-4 and human blood group antigens at the contact sites between these cells. By comparing the number of RBCs attaching to each tumor cell, we found that cells with high pre-incubation expression levels of galectin-4 attached significantly more RBCs than those with low expression levels (p < 1 × 10-7). Conversely, we found that RBC attachment induces galectin-4 expression in tumor cells. CONCLUSIONS: From our data we conclude that tumor cells directly interact with red blood cells via galectin-4.
BACKGROUND: The ability of tumor cells to invade and metastasize is relevant to the process of cancer progression and, as such, it represents an obstacle to cancer cure. So far, limited information is available on interactions between circulating tumor cells and blood cells. It is well-documented that galectin-4 is upregulated in many types of tumor cells and is involved in metastasis. Here, we address the hypothesis that tumor cells may interact with red blood cells (RBCs) via galectin-4. METHODS: High galectin-4 expressing colon, normal pancreatic and pancreatic cancer-derived cell lines (n = 5) were incubated with peripheral blood cells from different donors. Their interactions and associated proteins were examined by immunostaining and live cell imaging. RESULTS: We found that (endogenous or exogenous) galectin-4 expressing tumor cells interact directly with RBCs. We also observed an accumulation of galectin-4 and human blood group antigens at the contact sites between these cells. By comparing the number of RBCs attaching to each tumor cell, we found that cells with high pre-incubation expression levels of galectin-4 attached significantly more RBCs than those with low expression levels (p < 1 × 10-7). Conversely, we found that RBC attachment induces galectin-4 expression in tumor cells. CONCLUSIONS: From our data we conclude that tumor cells directly interact with red blood cells via galectin-4.
Entities:
Keywords:
Blood; Cancer cells; Erythrocytes; Galectin-4; Interactions
Authors: Hannah Barrow; Xiuli Guo; Hans H Wandall; Johannes W Pedersen; Bo Fu; Qicheng Zhao; Chen Chen; Jonathan M Rhodes; Lu-Gang Yu Journal: Clin Cancer Res Date: 2011-09-20 Impact factor: 12.531
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