Abstract
Cancer stem cells (CSCs) serve an important role in tumorigenesis, tolerance to treatment, relapse and metastasis. Although the signaling pathways involved in cancer are well known, the molecular mechanisms underlying CSC actions require further investigation. In the present study, a population of colon CSCs with a cluster of differentiation 133 (CD133) surface‑expression phenotype from the human SW480 colon adenocarcinoma cell line were isolated by flow cytometry. The CD133+ cells exhibited increased tumor sphere‑forming efficiency in vitro and increased tumorigenic potential in vivo. Furthermore, the gene expression profile of colon CSCs was investigated using gene chip technology. The results demonstrated differential gene expression between the CD133+ and CD133‑ subpopulations, including in relation to a number of important genes with functions in transcription control, cell cycle, karyomitosis and protein phosphorylation, including cyclin dependent kinase inhibitor 1A, cyclin B1, checkpoint kinase 1, cyclin dependent kinase 1 and transforming growth factor β receptor 2. Pathway analysis revealed that the mitogen‑activated protein kinase, p53 and calcium signaling pathways, as well as other important signaling pathways, were differentially activated between CD133+ and CD133‑ cells. To the best of our knowledge, these results provide the first evidence for the gene expression profile of colon CSCs in the SW480 colon adenocarcinoma cell line. Although further studies will be required to identify the functional roles of these genes in the CSC phenotype, these observations provide the basis for future studies to elucidate the pathogenesis of colorectal cancer and to develop novel tumor‑targeting therapies.
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