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Review
. 2019 Oct 24:9:1104.
doi: 10.3389/fonc.2019.01104. eCollection 2019.

Therapeutic Strategies Targeting Cancer Stem Cells and Their Microenvironment

Hao-Ran Sun  1 , Shun Wang  1 , Shi-Can Yan  1 , Yu Zhang  1 , Peter J Nelson  2 , Hu-Liang Jia  1 , Lun-Xiu Qin  1 , Qiong-Zhu Dong  1
Affiliations
Review

Therapeutic Strategies Targeting Cancer Stem Cells and Their Microenvironment

Hao-Ran Sun et al. Front Oncol. .

Abstract

Cancer stem cells (CSCs) have been demonstrated in a variety of tumors and are thought to act as a clonogenic core for the genesis of new tumor growth. This small subpopulation of cancer cells has been proposed to help drive tumorigenesis, metastasis, recurrence and conventional therapy resistance. CSCs show self-renewal and flexible clonogenic properties and help define specific tumor microenvironments (TME). The interaction between CSCs and TME is thought to function as a dynamic support system that fosters the generation and maintenance of CSCs. Investigation of the interaction between CSCs and the TME is shedding light on the biologic mechanisms underlying the process of tumor malignancy, metastasis, and therapy resistance. We summarize recent advances in CSC biology and their environment, and discuss the challenges and future strategies for targeting this biology as a new therapeutic approach.

Keywords: cancer stem cells; mechanism; strategy; therapeutic resistance; tumor microenvironments.

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Figures

Figure 1
Figure 1
Schematic illustration of the potential effects of hypoxia interaction on cancer stem cells (CSCs).
Figure 2
Figure 2
Schematic illustration of the potential effects of CAF interaction on cancer stem cells (CSCs).
Figure 3
Figure 3
Schematic representation of cancer stem cells (CSCs) and its role in therapeutic resistance. (A) Most of the cancer cells are eliminated by therapeutic resistance. CSC could escape from chemotherapy and re-establish tumor. (B) CSC possess several mechanisms to achieve therapeutic resistance involves Hypoxia environment, high expression of anti-apoptosis proteins, epithelial mesenchymal transition (EMT), DNA damaging repair system (DDR), multiple drug resistance transporters (MDR).
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