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Front. Biol.    2014, Vol. 9 Issue (2) : 114-126    https://doi.org/10.1007/s11515-014-1300-8
REVIEW
Priming cancer cells for drug resistance: role of the fibroblast niche
Wei Bin FANG,Min YAO,Nikki CHENG()
Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, USA
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Abstract

Conventional and targeted chemotherapies remain integral strategies to treat solid tumors. Despite the large number of anti-cancer drugs available, chemotherapy does not completely eradicate disease. Disease recurrence and the growth of drug resistant tumors remain significant problems in anti-cancer treatment. To develop more effective treatment strategies, it is important to understand the underlying cellular and molecular mechanisms of drug resistance. It is generally accepted that cancer cells do not function alone, but evolve through interactions with the surrounding tumor microenvironment. As key cellular components of the tumor microenvironment, fibroblasts regulate the growth and progression of many solid tumors. Emerging studies demonstrate that fibroblasts secrete a multitude of factors that enable cancer cells to become drug resistant. This review will explore how fibroblast secretion of soluble factors act on cancer cells to enhance cancer cell survival and cancer stem cell renewal, contributing to the development of drug resistant cancer.
Keywords fibroblasts      tumor recurrence      drug resistance      cell survival      stem cells      tumor dormancy     
Corresponding Author(s): Nikki CHENG   
Issue Date: 13 May 2014
 Cite this article:   
Wei Bin FANG,Min YAO,Nikki CHENG. Priming cancer cells for drug resistance: role of the fibroblast niche[J]. Front. Biol., 2014, 9(2): 114-126.
 URL:  
https://academic.hep.com.cn/fib/EN/10.1007/s11515-014-1300-8
https://academic.hep.com.cn/fib/EN/Y2014/V9/I2/114
Tumor typeIncreased recurrenceDecreased survivalReference
BreastDesmoplasia, increased expression of α-SMA and PDGFRDesmoplasia, increased expression of α- SMA and PDGFRHasebe et al., 2000; Paulsson et al., 2009
ProstateIncreased numbers of myofibroblasts, increased vimentin and α-SMA expression, decreased expression of desminIncreased numbers of myofibroblasts, increased vimentin expression, decreased desmin expressionAyala et al., 2003
LungIncreased expression of α- SMA and podoplaninIncreased podoplanin expressionKitano et al., 2010; Kaseda et al., 2013; Schoppmann et al., 2013
ColonDesmoplasia, increased numbers of myofibroblasts,increased α-SMA expressionDesmoplasia,increased numbers of myo-fibroblasts,increased expression of FSP1, α-SMA and FAPTsujino et al., 2007; Kojima et al., 2010; Herrera et al., 2013
Uterine/endometrialDesmoplasiaDesmoplasiaYasunaga et al., 2003; Khunamornpong et al., 2013
Urinary/ bladderDesmoplasiaDesmoplasiaSamaratunga et al., 2005
KidneyNo data availableIncreased expression of paladin,α-SMA, UPARAP, and galectin3Gupta et al., 2011; de Boer et al., 2012
MelanomaDesmoplasiaNo significant associationBusam, 2011
Oral, head and neckIncreased expression of α- SMA,Vimentin and DesminNAKawashiri et al., 2009; Marsh et al., 2011
LiverDesmoplasiaDesmoplasiaWang et al., 2013
PancreasIncreased FAP expressionIncreased FAP expressionCohen et al., 2008
OvaryIncreased FAP expressionFewer fibroblastsChen and Lee, 1984; Mhawech-Fauceglia et al., 2013
Tab.1  Histo-pathological features associating fibroblasts in the primary tumor with disease recurrence and decreased survival of patients with solid tumors
Soluble factorType of CAFReference
HGFBreast, prostate, lung, colon, uterine, bladder, melanoma,liver, oral, pancreas, ovarian*Seslar et al., 1993; Shimao et al., 1999; Guirouilh et al., 2000; Parr and Jiang, 2001; Uchida et al., 2001; Yoshida et al., 2002; Cohen et al., 2006; Wang et al., 2007; Chen et al., 2008; Kwon et al., 2013; Yu et al., 2013
CCL2Breast, prostate, lung, colon, melanoma, liver, oral, pancreasWong et al., 1998; Silzle et al., 2003; Eyman et al., 2009; Li et al., 2009; Mueller et al., 2010; Tjomsland et al., 2011; Wu et al., 2011; Liu et al., 2013
CXCL12Breast, prostate, lung, colon, liver, oral, pancreas, ovarianOrimo et al., 2005; Ohira et al., 2006; Daly et al., 2008; Addadi et al., 2010; Ibarra-Drendall et al., 2011; Chao et al., 2012; Feig et al., 2013
WNT16BProstateAhn et al., 2012
PeriostinBreast, prostate, lung, oral, liver, ovarianChoi et al., 2011; Li et al., 2012; Lv et al., 2013; Xu et al., 2012; Nuzzo et al., 2012; Hong et al., 2013
Tenascin CBreast, lung, colon, uterine, bladder, kidney, melanoma, liverahkola et al., 1998; Emoto et al., 2001; Buyukbayram and Arslan, 2002; Aishima et al., 2003; Brunner et al., 2004; Ilmonen et al., 2004; Ohno et al., 2008; JKahn et al., 2012
Tab.2  Carcinoma associated fibroblasts of solid tumors that express soluble factors associated with drug resistance
Fig.1  Role of fibroblast: cancer cell paracrine signaling interactions in the promotion of drug resistant tumors.

An important function of the fibroblast niche is to communicate with cancer cells directly, to enhance cell survival and cancer stem cell renewal. Carcinoma associated fibroblasts secrete a combination of growth factors, cytokines, and extracellular matrix related proteins including: HGF, WNT16B, CCL2 and CXCL12, Tenascin C and Periostin. Activity of these factors are modulated through different classes of receptors. HGF activity is mediated through receptor tyrosine kinases, while WNT16, CCL2 and CXCL12 binds to G protein coupled receptors. Tenascin C/Periostin protein complexes signal through integrin receptors. These factors activate MAPK, NF-kB and AKT pathways in cancer cells to promote survival and inhibit cell death. These soluble factors also promote renewal of cancer stem cells through similar pathways. These cellular and molecular processes contribute to the development and progression of drug resistant tumors.

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