Abstract
Cancer stem cells (CSCs) modify and form their microenvironment by recruiting and activating specific cell types such as mesenchymal stem cells (MSCs). Tumor-infiltrating MSCs help to establish a suitable tumor microenvironment for the restoration of CSCs and tumor progression. In addition, crosstalk between cancer cells and MSCs in the microenvironment induces a CSC phenotype in cancer cells. Many mechanisms are involved in crosstalk between CSCs/cancer cells and MSCs including cell-cell interaction, secretion of exosomes, and paracrine secretion of several molecules including inflammatory mediators, cytokines, and growth factors. Since this crosstalk may contribute to drug resistance, metastasis, and tumor growth, it is suggested that blockade of the crosstalk between MSCs and CSCs/cancer cells can provide a new avenue to improving the cancer therapeutic tools. In this review, we will discuss the role of MSCs in the induction of cancer stem cell phenotype and the restoration of CSCs. We also discuss targeting the crosstalk between MSCs and CSCs/cancer cells as a therapeutic strategy.
Highlights
Cancer stem cells (CSCs), which have been shown to play a vital role in tumor origin, are considered to be responsible for tumor progression, drug resistance, and metastasis [1]
Since crosstalk between tumor cells and mesenchymal stem cells (MSCs) may contribute to drug resistance, metastasis, and tumor growth, it is suggested that blockade of the crosstalk between MSCs and tumor cells can provide a new avenue to improving the cancer therapeutic tools
MSCs help to establish a suitable tumor microenvironment for the restoration of CSCs and tumor progression, as well as crosstalk between cancer cells and MSCs in the microenvironment induces a CSC phenotype in cancer cells. Since this communication can contribute to drug resistance, metastasis, and tumor growth, it is suggested that blockade of the crosstalk between MSCs and CSCs/ cancer cells can provide a new avenue to improving the cancer therapeutic tools
Summary
Cancer stem cells (CSCs), which have been shown to play a vital role in tumor origin, are considered to be responsible for tumor progression, drug resistance, and metastasis [1]. Many studies show the crosstalk between tumor cells and MSCs. For instance, transforming growth factor (TGF)-bstimulated MSCs can induce a metastatic phenotype by upregulating Jagged-1, a major ligand of Notch signaling, in tumor cells [4]. Activation of the Notch signaling pathway induces epithelial-mesenchymal transition (EMT) and promotes a cancer stem cell phenotype. This phenomenon is supported by other studies that show the relationship between the EMT process and CSCs [5]. In hepatocellular carcinoma, treating MSCs with tumor necrosis factor-a (TNF-a) and interferon g (IFNg) causes an increase in production of TGFb by MSCs which in turn could promote tumor metastasis by inducing EMT in cancer cells [6]. We discuss targeting the crosstalk between MSCs and CSCs/cancer cells as a therapeutic strategy
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