Tumor cells interact with red blood cells via galectin-4 - a short report

• Published in: Cellular oncology (Dordrecht) Vol. 40; no. 4; pp. 401 - 409
• Main Authors: Helwa, Reham, Heller, Anette, Knappskog, Stian, Bauer, Andrea S.
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer Netherlands 01.08.2017; Springer Nature B.V
• Subjects: Antigens; Biomedical and Life Sciences; Biomedicine; Blood; Cancer; Cancer Research; Cell Aggregation - genetics; Cell Communication - genetics; Cell Line, Tumor; Colon; Erythrocytes; Erythrocytes - cytology; Galectin 4 - genetics; Galectin 4 - metabolism; Gene Expression Regulation, Neoplastic; Humans; Immunohistochemistry; Metastases; Microscopy, Fluorescence; Neoplasms - genetics; Neoplasms - metabolism; Neoplasms - pathology; Oncology; Pancreatic cancer; Pathology; Peripheral blood; Reverse Transcriptase Polymerase Chain Reaction; Time-Lapse Imaging - methods; Tumor cell lines; Tumor cells; Interactions; Galectin-4; Blood; Erythrocytes; Cancer cells
• ISSN: 2211-3428; 2211-3436
• DOI: 10.1007/s13402-017-0317-9

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.