PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30089134-5 2018 Suppression or neutralization of the BZ-induced IL-8 potentiates the BZ cytotoxic and anti-proliferative effect in TNBC cells. Bortezomib 37-39 C-X-C motif chemokine ligand 8 Homo sapiens 48-52 30089134-5 2018 Suppression or neutralization of the BZ-induced IL-8 potentiates the BZ cytotoxic and anti-proliferative effect in TNBC cells. Bortezomib 69-71 C-X-C motif chemokine ligand 8 Homo sapiens 48-52 27301357-7 2016 In fact, the effect of bortezomib on IL-8 production was higher than that exerted by stromal-MM cell interactions. Bortezomib 23-33 C-X-C motif chemokine ligand 8 Homo sapiens 37-41 27455449-11 2016 Proteasome inhibitors, bortezomib and MG132, enhanced IL-8 production in both sides, apical and basolateral. Bortezomib 23-33 C-X-C motif chemokine ligand 8 Homo sapiens 54-58 27301357-6 2016 Interestingly, IL8 expression also increased in HMCLs, stromal cells, and osteoclasts after treatment with the antimyeloma drugs melphalan and bortezomib. Bortezomib 143-153 C-X-C motif chemokine ligand 8 Homo sapiens 15-18 25791477-0 2015 Anticancer drug bortezomib increases interleukin-8 expression in human monocytes. Bortezomib 16-26 C-X-C motif chemokine ligand 8 Homo sapiens 37-50 25791477-4 2015 Since monocytes and macrophages are major producers of IL-8, the goal of this study was to test the hypothesis that BZ increases the IL-8 expression in human monocytes and macrophages. Bortezomib 116-118 C-X-C motif chemokine ligand 8 Homo sapiens 55-59 25791477-4 2015 Since monocytes and macrophages are major producers of IL-8, the goal of this study was to test the hypothesis that BZ increases the IL-8 expression in human monocytes and macrophages. Bortezomib 116-118 C-X-C motif chemokine ligand 8 Homo sapiens 133-137 25791477-5 2015 Here, we show that BZ dramatically increases the IL-8 expression in lipopolysaccharide (LPS)-stimulated U937 macrophages as well as in unstimulated U937 monocytes and peripheral blood mononuclear cells, while it inhibits expression of IL-6, IL-1 and tumor necrosis factor-alpha. Bortezomib 19-21 C-X-C motif chemokine ligand 8 Homo sapiens 49-53 25791477-6 2015 In addition, our results show that the underlying mechanisms involve p38 mitogen-activated protein kinase, which is required for the BZ-induced IL-8 expression. Bortezomib 133-135 C-X-C motif chemokine ligand 8 Homo sapiens 144-148 25791477-7 2015 Together, these data suggest that the BZ-increased IL-8 expression in monocytes and macrophages may represent one of the mechanisms responsible for the BZ resistance and indicate that targeting the p38-mediated IL-8 expression could enhance the BZ effectiveness in cancer treatment. Bortezomib 38-40 C-X-C motif chemokine ligand 8 Homo sapiens 51-55 25791477-7 2015 Together, these data suggest that the BZ-increased IL-8 expression in monocytes and macrophages may represent one of the mechanisms responsible for the BZ resistance and indicate that targeting the p38-mediated IL-8 expression could enhance the BZ effectiveness in cancer treatment. Bortezomib 38-40 C-X-C motif chemokine ligand 8 Homo sapiens 211-215 25791477-7 2015 Together, these data suggest that the BZ-increased IL-8 expression in monocytes and macrophages may represent one of the mechanisms responsible for the BZ resistance and indicate that targeting the p38-mediated IL-8 expression could enhance the BZ effectiveness in cancer treatment. Bortezomib 152-154 C-X-C motif chemokine ligand 8 Homo sapiens 51-55 25791477-7 2015 Together, these data suggest that the BZ-increased IL-8 expression in monocytes and macrophages may represent one of the mechanisms responsible for the BZ resistance and indicate that targeting the p38-mediated IL-8 expression could enhance the BZ effectiveness in cancer treatment. Bortezomib 152-154 C-X-C motif chemokine ligand 8 Homo sapiens 51-55 24908314-3 2014 We have recently shown that proteasome inhibition by bortezomib (BZ) specifically increases IL-8 release from metastatic prostate and ovarian cancer cells. Bortezomib 53-63 C-X-C motif chemokine ligand 8 Homo sapiens 92-96 25661379-7 2015 Consistently, the combined exposure of romidepsin and bortezomib reversed the effects on IkappaB degradation as evident with IL-8, p50 and p65 (NF-kappaB) expression. Bortezomib 54-64 C-X-C motif chemokine ligand 8 Homo sapiens 125-129 25089799-7 2014 Bcl3 expression is regulated by bortezomib (BZ)-mediated proteasome inhibition, and BZ inhibits Bcl3 recruitment to its target promoters, resulting in decreased expression of cIAP1 and cIAP2, but increased expression of IL-8 and IL-17. Bortezomib 84-86 C-X-C motif chemokine ligand 8 Homo sapiens 220-224 24908314-3 2014 We have recently shown that proteasome inhibition by bortezomib (BZ) specifically increases IL-8 release from metastatic prostate and ovarian cancer cells. Bortezomib 65-67 C-X-C motif chemokine ligand 8 Homo sapiens 92-96 24908314-5 2014 IL-8 is localized in the cytoplasm in both cell types, and its protein levels are significantly increased by BZ. Bortezomib 109-111 C-X-C motif chemokine ligand 8 Homo sapiens 0-4 24908316-0 2014 Quantitative analysis of bortezomib-induced IL-8 gene expression in ovarian cancer cells. Bortezomib 25-35 C-X-C motif chemokine ligand 8 Homo sapiens 44-48 24908316-5 2014 We have recently shown that in ovarian cancer cells, BZ greatly increases IL-8 expression, while expression of other NFkappaB-regulated cytokines, IL-6 and TNF, is unchanged. Bortezomib 53-55 C-X-C motif chemokine ligand 8 Homo sapiens 74-78 24908316-6 2014 In this chapter, we describe a protocol that uses real-time qRT-PCR to quantitatively analyze mRNA levels of IL-8 and IL-6 in BZ-treated ovarian cancer cells. Bortezomib 126-128 C-X-C motif chemokine ligand 8 Homo sapiens 109-113 17172406-3 2006 Bortezomib synergized with IFN-alpha to promote apoptosis via a tumor necrosis factor-related apoptosis-inducing ligand-associated mechanism but did not inhibit production of proangiogenic factors (vascular endothelial growth factor, basic fibroblast growth factor, and interleukin-8) in human UM-UC-5 cells. Bortezomib 0-10 C-X-C motif chemokine ligand 8 Homo sapiens 270-283 23894194-0 2013 Proteasome inhibition by bortezomib increases IL-8 expression in androgen-independent prostate cancer cells: the role of IKKalpha. Bortezomib 25-35 C-X-C motif chemokine ligand 8 Homo sapiens 46-50 23894194-4 2013 In this article, we report that proteasome inhibition by BZ unexpectedly increases IL-8 expression in androgen-independent prostate cancer PC3 and DU145 cells, whereas expression of other NF-kappaB-regulated genes is inhibited or unchanged. Bortezomib 57-59 C-X-C motif chemokine ligand 8 Homo sapiens 83-87 23894194-5 2013 The BZ-increased IL-8 expression is associated with increased in vitro p65 NF-kappaB DNA binding activity and p65 recruitment to the endogenous IL-8 promoter. Bortezomib 4-6 C-X-C motif chemokine ligand 8 Homo sapiens 17-21 23894194-5 2013 The BZ-increased IL-8 expression is associated with increased in vitro p65 NF-kappaB DNA binding activity and p65 recruitment to the endogenous IL-8 promoter. Bortezomib 4-6 C-X-C motif chemokine ligand 8 Homo sapiens 144-148 23894194-6 2013 In addition, proteasome inhibition induces a nuclear accumulation of IkappaB kinase (IKK)alpha, and inhibition of IKKalpha enzymatic activity significantly attenuates the BZ-induced p65 recruitment to IL-8 promoter and IL-8 expression, demonstrating that the induced IL-8 expression is mediated, at least partly, by IKKalpha. Bortezomib 171-173 C-X-C motif chemokine ligand 8 Homo sapiens 201-205 23894194-6 2013 In addition, proteasome inhibition induces a nuclear accumulation of IkappaB kinase (IKK)alpha, and inhibition of IKKalpha enzymatic activity significantly attenuates the BZ-induced p65 recruitment to IL-8 promoter and IL-8 expression, demonstrating that the induced IL-8 expression is mediated, at least partly, by IKKalpha. Bortezomib 171-173 C-X-C motif chemokine ligand 8 Homo sapiens 219-223 23894194-6 2013 In addition, proteasome inhibition induces a nuclear accumulation of IkappaB kinase (IKK)alpha, and inhibition of IKKalpha enzymatic activity significantly attenuates the BZ-induced p65 recruitment to IL-8 promoter and IL-8 expression, demonstrating that the induced IL-8 expression is mediated, at least partly, by IKKalpha. Bortezomib 171-173 C-X-C motif chemokine ligand 8 Homo sapiens 219-223 23894194-7 2013 Together, these data provide the first evidence, to our knowledge, for the gene-specific increase of IL-8 expression by proteasome inhibition in prostate cancer cells and suggest that targeting both IKKalpha and the proteasome may increase BZ effectiveness in treatment of androgen-independent prostate cancer. Bortezomib 240-242 C-X-C motif chemokine ligand 8 Homo sapiens 101-105 22324515-9 2012 Interleukin-8 and vascular endothelial growth factor transcripts were induced after neuropeptides treatment, but downregulated by bortezomib. Bortezomib 130-140 C-X-C motif chemokine ligand 8 Homo sapiens 0-13 24085292-4 2013 However, we found that long-term incubation with PIs (PS-341 or MG132) increased NF-kappaB-regulated gene expression such as COX-2, cIAP2, XIAP, and IL-8 in a dose- and time-dependent manner, which was mediated by phosphorylation of IkappaBalpha and its subsequent degradation via the alternative route, lysosome. Bortezomib 54-60 C-X-C motif chemokine ligand 8 Homo sapiens 149-153 15026548-5 2004 Bortezomib also inhibited secretion of the proangiogenic factors matrix metalloproteinase-9, interleukin-8 (IL-8), and vascular endothelial growth factor (VEGF). Bortezomib 0-10 C-X-C motif chemokine ligand 8 Homo sapiens 93-106 15026548-5 2004 Bortezomib also inhibited secretion of the proangiogenic factors matrix metalloproteinase-9, interleukin-8 (IL-8), and vascular endothelial growth factor (VEGF). Bortezomib 0-10 C-X-C motif chemokine ligand 8 Homo sapiens 108-112 16621797-7 2006 Inhibition of the proteasome with bortezomib (PS-341/Velcade) also rescued CFTR, but with less efficiency, and suppressed NFkappaB-mediated IL8 activation. Bortezomib 34-44 C-X-C motif chemokine ligand 8 Homo sapiens 140-143 16621797-8 2006 The inhibition of the major stress-inducible transcription factor CHOP (CCAAT/enhancer-binding protein homologous protein)/GADD153 together with bortezomib was most effective in repressing NFkappaB-mediated IL8 activation compared with interference of VCP, MLN-273 (proteasome inhibitor), or 4-phenylbutyrate (histone deacetylase inhibitor). Bortezomib 145-155 C-X-C motif chemokine ligand 8 Homo sapiens 207-210 15514602-10 2004 RESULTS: Suberoylanilide hydroxamic acid significantly enhanced interleukin 8 and nuclear factor kappaB-dependent reporter gene transcription, and these effects were inhibited by bortezomib ( P < or = .01). Bortezomib 179-189 C-X-C motif chemokine ligand 8 Homo sapiens 64-122 12538487-8 2003 Inhibiting NFkappaB activation by expressing IkappaBalphaM and using pharmacologic NFkappaB inhibitor PS-341 also significantly reduced cytokine-induced vascular endothelial growth factor and interleukin-8 expression in AsPc-1 pancreatic cancer cells. Bortezomib 102-108 C-X-C motif chemokine ligand 8 Homo sapiens 192-205