Abstract
Even if cancer stem cells (CSCs) represent only a small proportion of the tumor mass, they significantly account for tumor maintenance, resistance to therapies, relapse and metastatic spread, due to their increased capacity of self-renewal, multipotency, tumorigenicity and quiescence. Emerging evidence suggests that the immune contexture within the tumor microenvironment (TME) determines both the response to therapy and the clinical outcome. In this context, CSCs acquire immune evasion skills by editing immune cell functions and sculpting the immunosuppressive landscape of TME. Reciprocally, infiltrating immune cells influence CSCs self-renewal, tumorigenicity and metastasis. In this review, we summarize the immunomodulatory properties of CSCs, as well as the impact of innate immune cells on cancer cells stemness in the different phases of cancer immunoediting process and neoplastic progression.
Highlights
The transformation of normal cells into a malignant tumor is a multistep process through which transforming cells acquire malignant features, described as “hallmarks of cancer”
We summarize the immunomodulatory properties of cancer stem cells (CSCs), as well as the impact of innate immune cells on cancer cells stemness in the different phases of cancer immunoediting process and neoplastic progression
In primary samples of acute myeloid leukemia, Shapiro’s group demonstrated that leukemia cells collected at tumor relapse had undergone a lower number of divisions, compare to cells collected at diagnosis, and presented features resembling the stem cell subset [78]. These results indicate that tumor growth is triggered by an aggressive and slowly dividing cancer cell clone, the CSCs, endowed with tolerogenic properties
Summary
The transformation of normal cells into a malignant tumor is a multistep process through which transforming cells acquire malignant features, described as “hallmarks of cancer”. These include sustaining proliferative signaling, evading anti-proliferative safeguards, resisting apoptotic programming, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. New observations indicate that the changes to which the transformed cells are subjected, including their heterogeneity and stemness, are affected by and mutually influence the host’s immune-inflammatory response, suggesting a model of tumor/host interdependence, in which the determinants of neoplastic progression are still largely unclear
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