Targeting metastasis-initiating cells through the fatty acid receptor CD36

被引:0
作者
Gloria Pascual
Alexandra Avgustinova
Stefania Mejetta
Mercè Martín
Andrés Castellanos
Camille Stephan-Otto Attolini
Antoni Berenguer
Neus Prats
Agustí Toll
Juan Antonio Hueto
Coro Bescós
Luciano Di Croce
Salvador Aznar Benitah
机构
[1] Institute for Research in Biomedicine (IRB Barcelona),Department of Dermatology
[2] The Barcelona Institute of Science and Technology (BIST),Department of Oral and Maxillofacial Surgery
[3] Centre for Genomic Regulation (CRG),undefined
[4] The Barcelona Institute of Science and Technology (BIST),undefined
[5] IMIM,undefined
[6] Hospital del Mar,undefined
[7] Vall D´Hebron Hospital,undefined
[8] Barcelona,undefined
[9] Universitat Autònoma de Barcelona,undefined
[10] Catalan Institution for Research and Advanced Studies (ICREA),undefined
[11] Universitat Pompeu Fabra (UPF),undefined
来源
Nature | 2017年 / 541卷
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摘要
The fact that the identity of the cells that initiate metastasis in most human cancers is unknown hampers the development of antimetastatic therapies. Here we describe a subpopulation of CD44bright cells in human oral carcinomas that do not overexpress mesenchymal genes, are slow-cycling, express high levels of the fatty acid receptor CD36 and lipid metabolism genes, and are unique in their ability to initiate metastasis. Palmitic acid or a high-fat diet specifically boosts the metastatic potential of CD36+ metastasis-initiating cells in a CD36-dependent manner. The use of neutralizing antibodies to block CD36 causes almost complete inhibition of metastasis in immunodeficient or immunocompetent orthotopic mouse models of human oral cancer, with no side effects. Clinically, the presence of CD36+ metastasis-initiating cells correlates with a poor prognosis for numerous types of carcinomas, and inhibition of CD36 also impairs metastasis, at least in human melanoma- and breast cancer-derived tumours. Together, our results indicate that metastasis-initiating cells particularly rely on dietary lipids to promote metastasis.
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页码:41 / 45
页数:4
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共 120 条
[31]  
Taichman RS(2011)Comparative studies of vertebrate platelet glycoprotein 4 (CD36) Metab. Syndr. Relat. Disord. 9 239-245
[32]  
Shiozawa Y(2004)Pathogenic role of scavenger receptor CD36 in the metabolic syndrome and diabetes Nat. Rev. Drug Discov. 3 695-710
[33]  
Prince ME(2006)Lipid metabolic enzymes: emerging drug targets for the treatment of obesity Invest. Ophthalmol. Vis. Sci. 47 4356-4364
[34]  
Harper LJ(2013)Activation of CD36 inhibits and induces regression of inflammatory corneal neovascularization Arterioscler. Thromb. Vasc. Biol. 33 1655-1662
[35]  
Piper K(2016)Molecular basis of antiangiogenic thrombospondin-1 type 1 repeat domain interactions with CD36 Sci. Rep. 6 18669-294
[36]  
Common J(2011)Genetic alterations in fatty acid transport and metabolism genes are associated with metastatic progression and poor prognosis of human cancers J. Exp. Biol. 214 286-260
[37]  
Fortune F(2015)Metabolic fuels: regulating fluxes to select mix Nature 525 256-2469
[38]  
Mackenzie IC(2015)Distinct EMT programs control normal mammary stem cells and tumour-initiating cells Cell Reports 13 2456-C638
[39]  
Biddle A(2015)Mesenchymal cancer cell-stroma crosstalk promotes niche activation, epithelial reversion, and metastatic colonization Am. J. Physiol. Cell Physiol. 309 C627-476
[40]  
Coburn CT(2015)Microenvironment in metastasis: roadblocks and supportive niches Nature 527 472-530