Cancer Stem Cells, Tumor Microenvironment and Nanomedicine

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Chemotherapy is one of the current mainstream anticancer therapies using chemicals to induce apoptosis by damaging DNA and/or inhibiting mitotic division to kill rapidly dividing cancer cells. Conventional chemotherapeutic strategy may exhibit initial success, but the eventual relapse of tumor growth is due to a greater resistance which recognized as the primary cause of chemotherapeutic failure for most human cancers. Because of genetic instability in cancer cells, nonrecurring mutations and large genomic alterations generate vast heterogeneity, giving rise to tumors which comprised subpopulations of distinct cells. Some of the tumor cells have been known as intrinsic resistance to the “achievable” doses of anticancer drugs, while other tumor cells are initially sensitive but become resistant during the course of treatment. There are three important chemo-resistant issues: 1) the pharmacological factor, which is the “inadequate” drug concentration at the tumor site, causes chemo-resistance; 2) cellular factor, which is a certain type of cancer cells, such as progenitor Cells/Cancer Stem Cells (CSCs), renders a capability for the subset of cancer cells evading slaughter of a variety of structurally and functionally chemo-agents 3) tumor microenvironment factor, which is dictated in one way or another, by a specific composition for tumor initiation and induction of tumoral angiogenesis, and for invasion and metastatic processes.

CSC and its niches CSCs, a sub population of tumor cells with the capabilities of self-renewal and differentiation potentials, contribute to tumor initiation, progression, and recurrence. CSC has been accepted as the most significant factor for the therapeutic failure. Although the mechanism is poorly understood, the CSCs, in fact, are protected physically by multiple lines of defense to resist chemotherapy. To resemble normal stem cells which generally located at places that are less exposed to potential external attacks, CSCs also take the maximal advantage of the CSC niches they are localized in. CSCs can differentiate into tumor cells under some circumstances, while the non-CSC-tumor cells may dedifferentiate into CSCs. Evidence suggests that CSCs and non-CSCs are not in amotion less but in a dynamic equilibrium state. The chemo-agents can kill the non-CSCs but may not the CSCs, especially those CSCs hidden in the CSCs niches.