5 research outputs found
Epigenetic alterations involved in cancer stem cell reprogramming
Current hypotheses suggest that tumors originate from cells that carry out a process of 'malignant reprogramming' driven by genetic and epigenetic alterations. Multiples studies reported the existence of stem-cell-like cells that acquire the ability to self-renew and are able to generate the bulk of more differentiated cells that form the tumor. This population of cancer cells, called cancer stem cells (CSC), is responsible for sustaining the tumor growth and, under determined conditions, can disseminate and migrate to give rise to secondary tumors or metastases to distant organs. Furthermore, CSCs have shown to be more resistant to anti-tumor treatments than the non-stem cancer cells, suggesting that surviving CSCs could be responsible for tumor relapse after therapy. These important properties have raised the interest in understanding the mechanisms that govern the generation and maintenance of this special population of cells, considered to lie behind the on/off switches of gene expression patterns. In this review, we summarize the most relevant epigenetic alterations, from DNA methylation and histone modifications to the recently discovered miRNAs that contribute to the regulation of cancer stem cell features in tumor progression, metastasis and response to chemotherapy
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In vitro models of cancer stem cells and clinical applications
Cancer cells, stem cells and cancer stem cells have for a long time played a significant role in the biomedical sciences. Though cancer therapy is more effective than it was a few years ago, the truth is that still none of the current non-surgical treatments can cure cancer effectively. The reason could be due to the subpopulation called “cancer stem cells” (CSCs), being defined as those cells within a tumour that have properties of stem cells: self-renewal and the ability for differentiation into multiple cell types that occur in tumours. The phenomenon of CSCs is based on their resistance to many of the current cancer therapies, which results in tumour relapse. Although further investigation regarding CSCs is still needed, there is already evidence that these cells may play an important role in the prognosis of cancer, progression and therapeutic strategy. Therefore, long-term patient survival may depend on the elimination of CSCs. Consequently, isolation of pure CSC populations or reprogramming of cancer cells into CSCs, from cancer cell lines or primary tumours, would be a useful tool to gain an in-depth knowledge about heterogeneity and plasticity of CSC phenotypes and therefore carcinogenesis. Herein, we will discuss current CSC models, methods used to characterize CSCs, candidate markers, characteristic signalling pathways and clinical applications of CSCs. Some examples of CSC-specific treatments that are currently in early clinical phases will also be presented in this review