A murine colorectal carcinoma (CRC) model was established. CT26 colon carcinoma cells
were injected into BALB/c mice's spleen to study the primary tumor and the mechanisms
of cell spread of colon cancer to the liver. The CRC was verified by the immunohistochemistry
of Pan Cytokeratin and Vimentin expression. Immunophenotyping of leukocytes isolated
from CRC-bearing BALB/c mice or healthy controls, such as CD19+ B cells, CD11+ myeloid
cells, and CD3+ T cells, was carried out using fluorochrome-labeled lectins. The binding
of six lectins to white blood cells, such as galectin-1 (Gal1), siglec-1 (Sig1), Sambucus
nigra lectin (SNA), Aleuria aurantia lectin (AAL), Phytolacca americana lectin (PWM),
and galectin-3 (Gal3), was assayed. Flow cytometric analysis of the splenocytes revealed
the increased binding of SNA, and AAL to CD3 + T cells and CD11b myeloid cells; and
increased siglec-1 and AAL binding to CD19 B cells of the tumor-bearing mice. The
whole proteomic analysis of the established CRC-bearing liver and spleen versus healthy
tissues identified differentially expressed proteins, characteristic of the primary
or secondary CRC tissues. KEGG Gene Ontology bioinformatic analysis delineated the
established murine CRC characteristic protein interaction networks, biological pathways,
and cellular processes involved in CRC. Galectin-1 and S100A4 were identified as upregulated
proteins in the primary and secondary CT26 tumor tissues, and these were previously
reported to contribute to the poor prognosis of CRC patients. Modelling the development
of liver colonization of CRC by the injection of CT26 cells into the spleen may facilitate
the understanding of carcinogenesis in human CRC and contribute to the development
of novel therapeutic strategies.
