Background Cancer remains one of the leading causes of death worldwide, despite the possibilities to detect early onset of the most common cancer types. The search for the optimal therapy is complicated by the cancer diversity within tumors and the unsynchronized development of cancerous cells. Therefore, it is necessary to characterize cancer cell populations after treatment has been applied, because cancer recurrence is not rare. In our research, we concentrated on small cancer cell subpopulation (microcells) that has a potential to be cancer resistance source. Previously made experiments has shown that these cells in small numbers form in specific circumstances after anticancer treatment. Methods In experiments described in this research, the anticancer agents’ paclitaxel and doxorubicin were used to stimulate the induction of microcells in fibroblast, cervix adenocarcinoma, and melanoma cell lines. Mainly for the formation of microcells in melanoma cells. The drug-stimulated cells were then characterized in terms of their formation efficiency, morphology, and metabolic activity. Results We observed the development of cancer microcells and green fluorescent protein (GFP) transfection efficiency after stress. In the time-lapse experiment, we observed microcell formation through a renewal process and GFP expression in the microcells. Additionally, the microcells were viable after anticancer treatment, as indicated by the nicotinamide adenine dinucleotide hydrogen phosphate (NADPH) enzyme activity assay results. Taken together, these findings indicate that cancer microcells are viable and capable of resisting the stress induced by anticancer drugs, and these cells are prone to chemical substance uptake from the environment. Conclusion Microcells are not only common to a specific cancer type, but can be found in any tumor type. This study could help to understand cancer emergence and recurrence. The appearance of microcells in the studied cancer cell population could be an indicator of the individual anticancer therapy effectiveness and patient survival.
and genes, and usage of the same signaling pathways. At the same time, differences among normal and CSC lies in ability of the latter to metastastatic ability, tumorigenic activities and resistance to chemotherapy (24). Breast cancer stem cells are thought to be identifiable possessing markers CD44+/CD24 -/low . However, their numbers vary significantly among tumors, they are not regarded as specific for BCSC, rather for certain histological type (4). They are characterized by CD44+/ CD24 -/low /ESA+ markers, and lineage (lack of expression CD2, CD3, CD10, CD16, CD18, CD31, CD64 and CD 140b). As few as 200 of these subpopulation of cells are able to form tumors injected into NOD/SCID mice, and CD44+/CD24-phenotype has been used extensively to identify cancer cells known for they capability to give rise to tumors in mice. Breast tumor cells positive for ALDH are able to generate tumors with phenotype resembling parental one, therefore CD44+/ CD24-/ALDH+ phenotype increases even more the tumorigenicity of breast cancer cells, in comparison with CD44+/CD24-or ALDH+ alone (10). As far as experimental models are clarified, it seems not to be so clear-cut in human breast cancers (27). Nevertheless, BCSC seems to be intriguing topic for prognostic and predictive purposes in breast cancer.
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