A lack of investigation exists regarding the role and function of the cancer stem cell (CSC) populations In this thesis, methods were developed for selectively enriching CSC populations to allow for drug targeting studies. SW480 and CT26 parental wild-type (WT) colorectal cancer cells were transfected with a vector encoding the octamer-binding transcription factor 4 (OCT4) promoter site regulating the expression of enhanced green fluorescent protein (GFP). After repeated cell sorting (top ~1–5%), the highly positive OCT4-GFP populations were further enriched by using conditions of intermittent cycling between normoxia and anoxia. The resulting highly enriched OCT4-GFP CSC population produced markedly, more tumours of larger sizes compared to CT26 WT inoculated mice. Celecoxib treatment significantly decreased (~50%) the number and volume of colorectal tumours of both WT and CSC cell type. Colorectal tumours produced significant red blood cell levels in the peritoneal cavities of untreated mice, but celecoxib treatment greatly inhibited peritoneal tumour angiogenesis. Studies using these model systems will help determine the role of CSC-enriched populations in tumour progression and therapeutic targeting. The evidence also supports the potential for repurposing and using celecoxib in chemosensitising colorectal cancer cells, rendering them more susceptible to standard chemotherapies, such as doxorubicin and 5-fluorouracil.