Lectin-Based Immunophenotyping and Whole Proteomic Profiling of CT-26 Colon Carcinoma Murine Model.
Anna FaragóÁgnes ZvaraLászló TiszlaviczEva Hunyadi-GulyasZsuzsanna DarulaZoltán HegedűsEnikő SzabóSára Eszter SurgutaJózsef TóváriLászló G PuskásLászló G PuskásPublished in: International journal of molecular sciences (2024)
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.
Keyphrases
- induced apoptosis
- poor prognosis
- cell cycle arrest
- computed tomography
- gene expression
- endoplasmic reticulum stress
- dendritic cells
- single cell
- bone marrow
- contrast enhanced
- magnetic resonance imaging
- endothelial cells
- signaling pathway
- cell death
- magnetic resonance
- skeletal muscle
- binding protein
- patient reported outcomes
- transcription factor
- ejection fraction
- genome wide
- immune response
- insulin resistance
- small molecule
- wild type
- copy number
- peritoneal dialysis