##< 0

##< 0.01 versus GEM solitary treatment group. the proliferation, invasion and metastasis of pancreatic malignancy cells, induced cell apoptosis via oxidative stress, and enhanced GEM level of sensitivity by inhibiting the NF-B signaling pathway. Beyond that, experiments showed that DET not only inhibited pancreatic tumor growth and metastasis but also amplified the antitumor capacity of GEM, which was related to the downregulation of NF-B and its downstream gene products. In summary, it is possible that DET could be developed as a single agent or combined with standard chemotherapy drugs to improve the treatment of pancreatic malignancy. and < 0.05, **< 0.01 versus CTL. CTL, control. (E) Colony formation capacities of BxPC-3 and CFPAC-1 cells after DET treatment were evaluated by colony formation assays. **< 0.01 versus CTL. CTL, control. (F) Effect of DET within the migration capabilities of BxPC-3 and CFPAC-1 cells were recognized by wound healing assays. **< 0.01 versus CTL. CTL, control. (G, H) Effect of DET within the migration and invasive capabilities of BxPC-3 and CFPAC-1 cells were measured using Transwell assay. **< 0.01 versus CTL. CTL, control. Magnification, 40 (F), 200 (G, H). Level pub, 500 m (F), 100 m (G, H). DET, deoxyelephantopin. GEM, gemcitabine. DET inhibits the migration and invasion of BxPC-3 and CFPAC-1 cells < 0.05, **< 0.01 versus CTL. ##< 0.01 versus DET (50 M) at 2 h or DET (60 M) at 3 h. CTL, control. (D) Effect of DET on MMP in BxPC-3 and CFPAC-1 cells were tested using JC-1 probe and evaluated using fluorescence microplate reader. **< 0.01 versus CTL. ##< 0.01 versus DET (30 M) or DET (40 M). CTL, control. (E) Effect of DET on oxidative stress were further assessed using MitoSOX and observed under fluorescent microscope. 2-hexadecenoic acid (F) Effect of DET on fluorescence intensity of MitoSOX were recognized using fluorescence microplate reader. **< 0.01 versus CTL. #< 0.05 versus DET single treatment groups. CTL, control. (GCI) Effect of DET on intracellular GSH, GSSG and the percentage of GSH to GSSG in BxPC-3 and CFPAC-1 cells were assessed using GSSG/GSH quantification kit. *< 0.05, **< 0.01 versus CTL. CTL, control. (J) Effect of DET on intracellular TrxR activity was measured using thioredoxin reductase assay kit. **< 0.01 versus CTL. CTL, control. Magnification, 100 (A), 200 (B, E). Level pub, 200 m (A), 100 m (B, E). DCFH-DA, 2, 7-dichlorofluorescein-diacetate. GSH, reduced glutathione. GSSG, oxidative form of glutathione. TrxR, thioredoxin reductase. DET induces oxidative stress and interferes with MMP in BxPC-3 and CFPAC-1 cells < 0.01 versus CTL. CTL, control. (B) DET-induced apoptosis in BxPC-3 and CFPAC-1 cells were assessed using Hoechst 33342 staining. **< 0.01 versus CTL. ##< 0.01 versus DET (30 M) or DET (40 M). CTL, control. (C) DET-induced apoptosis in BxPC-3 and CFPAC-1 cells were identified using Annexin V-FITC/PI double staining. Annexin V-FITC (-) and PI (-) cells were defined as alive, Annexin V-FITC (+) but PI (-) cells were defined as early apoptosis, Annexin V-FITC (+) but PI (+) cells were considered to be late apoptosis. Annexin V-FITC (-) and PI (+) cells were thought to be necrotic cells. The total apoptosis rate was the sum of early apoptosis rate and late apoptosis rate. **< 0.01 versus CTL. ##< 0.01 versus DET (30 M) or DET (40 M). CTL, control. Magnification, 200 2-hexadecenoic acid (A, B). Level pub, 100 m (A, B). A circulation cytometric assay was applied to further evaluate DET-induced apoptosis. The data showed that DET induced apoptosis in BxPC-3 TGFbeta and CFPAC-1 cells with dependence on concentration. In addition, pretreating cells with NAC significantly reversed apoptosis, which implied that DET controlled apoptosis primarily by inducing oxidative stress (Number 3C). DET regulates Bcl-2 family protein expression levels and induces caspase cascade reaction < 0.05, **< 2-hexadecenoic acid 0.01 versus CTL. CTL, control. As caspase-9 and caspase-3 are downstream important transporters and executors of the mitochondrial apoptosis pathway and are triggered by cleavage, the cleaved.