Abstract
The recognition of intra-tumoral cellular heterogeneity has given way to the concept of the cancer stem cell (CSC). According to this concept, CSCs are able to self-renew and differentiate into all of the cancer cell lineages present within the tumor, placing the CSC at the top of a hierarchical tree. The observation that these cells—in contrast to bulk tumor cells—are able to exclusively initiate new tumors, initiate metastatic spread and resist chemotherapy implies that CSCs are solely responsible for tumor recurrence and should be therapeutically targeted. Toward this end, dissecting and understanding the biology of CSCs should translate into new clinical therapeutic approaches. In this article, we review the CSC concept in cancer, with a special focus on hepatocellular carcinoma.
Highlights
In solid tumor oncology, there are only few examples of medical treatments that are curative or that achieve sustained and long-term remission
The use of CXCR4 as a marker to identify metastatic cancer stem cell (CSC) is in line with previous studies in pancreatic cancer, in which we showed that CD133+/CXCR4+ CSCs have exclusive tumorigenic and metastasis-initiating capacity [9]
Several lines of evidence point to the CSC as a key therapeutic target in Hepatocellular carcinoma (HCC), as in many other tumors. This population must be successfully eliminated in order to prevent metastatic spread and tumor relapse, but due to their high therapy resistance and high cellular plasticity, effective means still have to be found to identify these cells and to adequately target them, especially in HCC
Summary
There are only few examples of medical treatments that are curative or that achieve sustained and long-term remission. This can lead to therapy-induced selection of a dominant clone with new biological features, and to the loss of those cells that were “addicted” to the previous molecular target, as has been observed with anti-EGFR (epithelial growth factor receptor) therapy in colorectal carcinoma [2] While clinical observations such as acquired drug resistance or tumor relapse can be explained by the clonal evolution model, evidence to the contrary exists. The authors demonstrated that CD34+/CD38− AML cells had significantly higher tumorigenic potential in SCID mice than the CD34+/CD38+ or CD34− fractions This discovery of intra-tumoral heterogeneity and tumor hierarchy led to the advent of the cancer stem cell (CSC) concept, with a CSC being a tumor cell that can self-renew, differentiate into all tumor cell lineages, exhibit exclusive tumor-initiating capacity and possess high chemotherapeutic resistance [5]. We will summarize the role of CSCs in cancer, and provide an overview of the current knowledge of CSCs in HCC
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