Trastuzumab　resistance　is　leading　cause　of　mortality　in　HER2-positive　breast　cancers,　and　the　role　of　TGF-β-induced　epithelial-mesenchymal　transition　(EMT)　in　trastuzumab　resistance　is　well　established,　but　the　involvement　of　lncRNAs　in　trastuzumab　resistance　is　still　unknown.　Here,　we　generated　trastuzumab-resistant　breast　cancer　cells　with　increased　invasiveness　compared　with　parental　cells,　and　observed　robust　epithelial-mesenchymal　transition　(EMT)　and　consistently　elevated　TGF-β　signaling　in　these　cells.　We　identified　long　noncoding　RNA　activated　by　TGF-β　(lnc-ATB)　was　the　most　remarkably　upregulated　lncRNA　in　TR　SKBR-3　cells　and　the　tissues　of　TR　breast　cancer　patients.　We　found　that　lnc-ATB　could　promote　trastuzumab　resistance　and　invasion-metastasis　cascade　in　breast　cancer　by　competitively　biding　miR-200c,　up-regulating　ZEB1　and　ZNF-217,　and　then　inducing　EMT.　In　addition,　we　also　found　that　the　high　level　of　lnc-ATB　was　correlated　with　trastuzumab　resistance　of　breast　cancer　patients.　Thus,　these　findings　suggest　that　lncRNA-ATB,　a　mediator　of　TGF-β　signaling,　could　predispose　breast　cancer　patients　to　EMT　and　trastuzumab　resistance.