Patient　SE　translation　(　SET)　is　a　carcinogen　in　facilitating　cellular　growth　and　proliferation,　and　promoting　tumorigenesis　and　metastasis.　The　present　study　was　to　investigate　the　resistance　mechanisms　associated　with　SET　in　paclitaxel-induced　human　breast　cancer　cells.　The　different　expressions　of　SET,　ATP-binding　cassette　(ABC)　transporters　and　PI3K/Akt　pathway　between　paclitaxel　sensitive　MCF-7/S　and　paclitaxel　resistant　MCF-7/PTX　cells　were　identified　using　western　blotting.　We　adopted　plasmid　transfection　to　upregulate　SET　in　MCF-7/S　cells　and　a　novel　SET　antagonist　COG112　to　decrease　SET　in　MCF-7/PTX　cells.　Subsequently,　cell　viability　to　paclitaxel　was　assessed　by　MTT　assay　and　cell　apoptosis　was　analyzed　by　flow　cytometry.　We　found　that　levels　of　SET,　ABC　transporters　and　PI3K/Akt　pathway　were　elevated　in　MCF-7/PTX.　Upregulation　of　SET　in　MCF-7/S　cells　expressed　resistant　to　paclitaxel　and　decreased　cell　apoptosis.　Moreover,　overexpression　of　SET　promoted　the　mRNA　and　protein　level　of　ABC　transporters　and　PI3K/Akt　signal　pathway　in　MCF-7/S　cells.　Conversely,　decreased　level　of　SET　by　COG112　not　only　significantly　sensitized　MCF-7/PTX　cells　to　paclitaxel,　but　also　enhanced　paclitaxel-induced　cell　apoptosis.　Additionally,　the　levels　of　the　ABC　transporters　and　PI3K/Akt　signal　pathway　were　also　reduced　in　the　COG112-treated　MCF-7/PTX　cells.　The　above　results　demonstrated　that　SET　was　associated　with　paclitaxel　resistance　in　MCF-7/PTX　cells.