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Journal of Hematology and Oncology

, 7:14

First Online: 06 February 2014Received: 15 November 2013Accepted: 31 December 2013DOI: 10.1186-1756-8722-7-14

Cite this article as: Sun, Z., Wang, S. & Zhao, R.C. J Hematol Oncol 2014 7: 14. doi:10.1186-1756-8722-7-14

Abstract

Tumor behavior is not entirely determined by tumor cells. Studies have demonstrated that a variety of non-tumor cells in the tumor microenvironment affect tumor behavior; thus, a new focus of cancer research has been the development of novel cancer treatment ideas and therapeutic targets based on the effects of these cells. Mesenchymal stem cells MSCs are an important component of the tumor microenvironment; however, previous studies have produced controversial results regarding whether MSCs promote or inhibit tumor growth and progression. In particular, Naïve MSCs and tumor-derived MSCs T-MSCs have different functions. Naïve MSCs could exert bidirectional effects on tumors because these cells can both promote and inhibit tumor progression while T-MSCs promote tumor progression due to influences from the tumor itself and from the inflammatory tumor microenvironment. As an unhealed wound, tumor produces a continuous source of inflammatory mediators and causes aggregation of numerous inflammatory cells, which constitute an inflammatory microenvironment. Inflammatory factors can induce homing of circulating MSCs and MSCs in adjacent tissues into tumors, which are then being -educated- by the tumor microenvironment to support tumor growth. T-MSCs could recruit more immune cells into the tumor microenvironment, increase the proportion of cancer stem cells and promote tumor angiogenesis, further supporting tumor progression. However, as plasti city is a fundamental feature of MSCs, MSCs can also inhibit tumors by activating various MSC-based signaling pathways. Studies of the mechanisms by which interactions among tumors, MSCs, and the inflammatory microenvironment occur and methods to disrupt these interactions will likely reveal new targets for cancer therapy.

KeywordsMesenchymal stem cell Tumor Inflammatory microenvironment AbbreviationsAMSCAdipose derived mesenchymal stem cell

BAMBBone morphogenetic protein and activin membrane-bound inhibitor

CCL5Chemokine C-C motif Ligand 5

CCRC-C chemokine receptor

CXCRchemokine C-X-C motif receptor

CXCLc-x-c motif chenokine

DCDendritic cells

ECEndothelial cell

EMTEpithelial-mesenchymal transition

ERKExtracellular signal-regulated kinase

ET-1Endothelin-1

FAKsFocal adhesion kinases

HIF-1Hypoxia inducible factor 1

IDOIndolamin2,3-dioxygenase

ILInterleukin

IFN-γInterferon-γ

Jak2Janus kinase 2

MAPKMitogen activated protein kinase

MDSCMyeloid-derived suppressor cells

MMPMatrix metalloproteinase

MSCMesenchymal stem cell

NK cellsNatural killer cells

NF-kBNuclear factor-kappa B

N-MSCNative mesenchymal stem cell

PGE2Prostaglandin E2

PGFPlacental growth factor

SDF-1Stromal cell-derived factor-1-alpha

STAT3Signal tranducers and transcription activators 3

SMASmooth muscle actin

TAFTumor related fibroblasts

TGF-βTransforming growth factor-beta

TLRToll-like receptor

T-MSCTumor derived mesenchymal stem cell

TNF-αTumor necrosis factor-α

VCAMVasculaer cell adhersion molecule

VEGFVascular endothelial growth factor.

Electronic supplementary materialThe online version of this article doi:10.1186-1756-8722-7-14 contains supplementary material, which is available to authorized users.

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Author: Zhao Sun - Shihua Wang - Robert Chunhua Zhao

Source: https://link.springer.com/







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