Metadherin Mediates Lipopolysaccharide-Induced Migration and Invasion of Breast Cancer Cells 英文参考文献.docVIP
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Metadherin Mediates Lipopolysaccharide-Induced Migration and Invasion of Breast Cancer Cells 英文参考文献
MetadherinMediatesLipopolysaccharide-Induced
MigrationandInvasionofBreastCancerCells
YuhanZhao1.,XiaoliKong1.,XiaoyanLi1,ShiYan2,CunzhongYuan2,WenweiHu3*,QifengYang1*
1DepartmentofBreastSurgery,ShandongUniversitySchoolofMedicine,Jinan,Shandong,China,2DepartmentofObstetricsandGynecology,QiluHospital,Shandong
UniversitySchoolofMedicine,Jinan,Shandong,China,3CancerInstituteofNewJersey,UniversityofMedicineandDentistryofNewJersey,NewBrunswick,NewJersey,
UnitedStatesofAmerica
Abstract
Background:Breastcanceristhemostprevalentcancerinwomenworldwideandmetastaticbreastcancerhasverypoor
prognosis.Inflammationhasbeenimplicatedinmigrationandmetastasisofbreastcancer,althoughtheexactmolecular
mechanismremainselusive.
PrincipalFindings:Weshowthatthepro-inflammatoryendotoxinLipopolysaccharide(LPS)upregulatestheexpressionof
Metadherin (MTDH), a recently identified oncogene, in a number of breast cancer lines. Stable knockdown of MTDH by
shRNAinhumanbreastMDA-MB-231cellsabolishesLPS-inducedcellmigrationandinvasionasdeterminedbyseveralin
vitroassays.Inaddition,knockdownofMTDHdiminishesNuclearFactor-kappaB(NF-kB)activationbyLPSandinhibited
LPS-inducedIL-8andMMP-9production.
Conclusions:TheseresultsstronglysuggestthatMTDHisapivotalmoleculeininflammation-mediatedtumormetastasis.
SinceNF-kB,IL-8andMMP-9playrolesinLPS-inducedinvasionormetastasis,themechanismofMTDH-promotedinvasion
andmetastasismaybethroughtheactivationofNF-kB,IL-8andMMP-9,alsosuggestingaroleofMTDHinregulatingboth
inflammatory responses and inflammation-associated tumor invasion. These findings indicate that MTDH is involved in
inflammation-induced tumor progression, and support that MTDH targeting therapy may hold promising prospects in
treatingbreastcancer.
Citation:ZhaoY,KongX,LiX,YanS,YuanC,etal.(2011)MetadherinMediatesLipopolysaccharide-InducedMigrationandInvasionofBreastCancerCells.PLoS
ONE6(12):e29363.doi:10.1371/journal.pone.0029363
Editor:JunLi,SunYat-senUniversityMedicalSchool,China
ReceivedAugust10,2011;Accepte
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