In 2018, the World Health Organization confirmed that cancer was responsible for 9.6 million deaths worldwide, and data also indicate that despite the availability of various drugs, their efficacy requires further improvement with a focus on the complexity of cancer.
It is now clear that cancer stem cells (CSCs) represent a small population of cancer cells within a tumor, and that they have typical properties associated with stem cells. Like their stem cell counterparts, CSCs possess “stem” properties reflected in their ability to self-renew and generate differentiated cells that contribute to tumor heterogeneity.
CSCs appear to arise from mutations affecting adult stem cells that are the source of organogenesis and tissue homeostasis. Despite ongoing debates about their origin, there is an urgent and ongoing need to better understand the function of CSCs in cancer initiation and progression, and most importantly, to develop CSC-specific targeting strategies.
Chemotherapy induces programmed cell death by damaging DNA and inhibiting mitosis, however, this treatment option is valid for highly dividing cancer cells and therefore has the potential to “overlook” slow-dividing cells, leading to cancer relapse and recurrence in treated patients. Unfortunately, follow-up chemotherapy that attempts to destroy resistant cancer cells has often been unsuccessful and has been associated with poor survival rates for treated cancer patients. Due to their slow rate of division, cancer stem cells mediate chemoresistance and recurrence after chemotherapy; however, additional mechanisms that confer a survival advantage on cancer stem cells include expression of ATP-binding cassette (ABC) transporters, higher expression of aldehyde dehydrogenases (ALDHs), increased resistance to apoptosis, and timely activation of the DNA damage sensor.
