Abstract
Cancer stem cells (CSCs), or cancer cells with stem cell-like properties, generally exhibit drug resistance and have highly potent cancer inducing capabilities. Genome-wide expression data collected at public repositories over the last few years provide excellent material for studies that can lead to insights concerning the molecular and functional characteristics of CSCs. Here, we conducted functional genomic studies of CSC based on fourteen PCA-screened high quality public CSC whole genome gene expression datasets and, as control, four high quality non-stem-like cancer cell and non-cancerous stem cell datasets from the Gene Expression Omnibus database. A total of 6,002 molecular signatures were taken from the Molecular Signatures Database and used to characterize the datasets, which, under two-way hierarchical clustering, formed three genotypes. Type 1, consisting of mainly glia CSCs, had significantly enhanced proliferation, and significantly suppressed epithelial-mesenchymal transition (EMT), related functions. Type 2, mainly breast CSCs, had significantly enhanced EMT, but not proliferation, related functions. Type 3, composed of ovarian, prostate, and colon CSCs, had significantly suppressed proliferation related functions and mixed expressions on EMT related functions.
Highlights
Cancer stem cells (CSCs), or cancer cells with stem cell-like properties, generally exhibit drug resistance and have highly potent cancer inducing capabilities
Our results indicate that in functional genomic terms the 14 cancer stem cells (CSCs) datasets fell into three genotypes
individual gene-based analysis (IGA) based on differentially expressed genes (DEGs) and Gene Set Enrichment Analysis (GSEA) based on enriched molecular signatures are fundamentally different approaches to genome representation
Summary
Cancer stem cells (CSCs), or cancer cells with stem cell-like properties, generally exhibit drug resistance and have highly potent cancer inducing capabilities. Potential causes of mutation include externally or internally induced DNA damage leading to mutations in protein coding genes, abnormal oncogene activation, and loss of activity in suppressor-genes An aggregation of such mutations can lead to the formation of cancer cells, and possibly to tumor formation[1]. The hypothesis that some cancer cells may have stem cell-like properties was first put forward by Furth and Kahn in 1937, who showed that a single transplanted leukemic cell was able to transmit the systemic disease to a mouse[2] This hypothesis did not receive substantial support until 1994, when it was shown that only select purified tumor cells with specific markers from acute myeloid leukemia (AML) patients could induce cancer when transplanted into a mouse[3]. A minute fraction of tumor cells have the conjoined properties of self-renewal, drug-resistance, and cancer-inducement Such cells have been commonly referred to as cancer stem cells (CSCs). Following a growing number of reports on CSCs in multiple types of cancers, the CSC hypothesis is receiving increasingly wider acceptance[4,5]
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