PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30292410-5 2018 Cell apoptosis was dramatically promoted in MM cells following silencing of ANXA1 and BTZ administration versus that in ANXA1-silenced alone or BTZ-treated alone cells, as evidenced by decreased expression of phosphorylated signal transducers and activators of transcription 3 and BCL2, and increased expression of BAX. Bortezomib 86-89 BCL2 associated X, apoptosis regulator Homo sapiens 315-318 29291406-6 2018 Among the inhibitors tested, only bortezomib and carfilzomib were able to induce differential cell death corresponding to the distinct Bax statuses. Bortezomib 34-44 BCL2 associated X, apoptosis regulator Homo sapiens 135-138 25602436-4 2015 Western blot showed that the Bortezomib strongly increased the levels of p-JNK, caspase-3, PARP, and bax proteins while it increased the level of bcl-2. Bortezomib 29-39 BCL2 associated X, apoptosis regulator Homo sapiens 101-104 28912868-7 2017 However, Bax-/- HCT116 cells became more resistant to apoptosis when treated with Velcade. Bortezomib 82-89 BCL2 associated X, apoptosis regulator Homo sapiens 9-12 25975837-0 2015 ALK-negative anaplastic large cell lymphoma is sensitive to bortezomib through Noxa upregulation and release of Bax from Bcl-2. Bortezomib 60-70 BCL2 associated X, apoptosis regulator Homo sapiens 112-115 27769058-9 2016 Bortezomib up-regulated pro-apoptotic proteins of the Bcl-2 protein family, Bax and Noxa in wild-type HCC cells. Bortezomib 0-10 BCL2 associated X, apoptosis regulator Homo sapiens 76-79 26956626-11 2016 CML cells exposed to bortezomib leads to conformational changes in Bax protein, resulting in loss of mitochondrial membrane potential and leakage of cytochrome c to the cytosol. Bortezomib 21-31 BCL2 associated X, apoptosis regulator Homo sapiens 67-70 25995634-9 2015 Furthermore, the combination of BTZ-GA/MNPs activated phosphorylated Akt levels, Caspase-3, and Bax expression, and down-regulated the PI3K and Bcl-2 levels significantly. Bortezomib 32-35 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 23179179-7 2013 In addition, we report that Bax-deficient HCT116 cells exposed to TRAIL for a prolonged period lost their sensitivity to TRAIL as a result of downregulation of TRAIL receptor expression, and became resistant to combination of TRAIL and other drugs such as MG-132 and bortezomib. Bortezomib 267-277 BCL2 associated X, apoptosis regulator Homo sapiens 28-31 24486574-5 2014 The combinational treatment of oxaliplatin and bortezomib promoted the JNK-Bcl-xL-Bax pathway which modulated the synergistic effect through the mitochondria-dependent apoptotic pathway. Bortezomib 47-57 BCL2 associated X, apoptosis regulator Homo sapiens 82-85 23481040-9 2013 Apoptotic activity of the proteasome inhibitor bortezomib was also related to Bax activation and P70S6K downregulation. Bortezomib 47-57 BCL2 associated X, apoptosis regulator Homo sapiens 78-81 23300762-2 2012 We have previously found that resistance to the proteasome inhibitor bortezomib in 3D can be explained by a lack of upregulation of Noxa, the pro-apoptotic BH3 sensitizer that acts via displacement of the Bak/Bax-activator BH3-only protein, Bim. Bortezomib 69-79 BCL2 associated X, apoptosis regulator Homo sapiens 209-212 22086447-7 2013 Our results also revealed that combination of bortezomib with vorinostat enhanced apoptosis by increasing Mcl-1 cleavage, Noxa upregulation, Bak and Bax activation, and cytochrome c release. Bortezomib 46-56 BCL2 associated X, apoptosis regulator Homo sapiens 149-152 22393246-0 2012 ABT-737 synergizes with bortezomib to induce apoptosis, mediated by Bid cleavage, Bax activation, and mitochondrial dysfunction in an Akt-dependent context in malignant human glioma cell lines. Bortezomib 24-34 BCL2 associated X, apoptosis regulator Homo sapiens 82-85 22393246-8 2012 Genetic and pharmacological inhibition of PI3K inhibition sensitized PTEN-deficient glioma cells to bortezomib- and ABT-737-induced apoptosis by increasing cleavage of Bid protein, activation and oligomerization of Bax, and loss of mitochondrial membrane potential. Bortezomib 100-110 BCL2 associated X, apoptosis regulator Homo sapiens 215-218 23226303-8 2012 Mechanistic studies of apoptotic pathways indicated that bortezomib induced activation of p53 and Bax, as well as cleavage of caspases and poly-ADP-ribose polymerase (PARP) in exposed chondrocytes. Bortezomib 57-67 BCL2 associated X, apoptosis regulator Homo sapiens 98-101 22169296-4 2011 The results showed that compared with cells treated with 2-ME2 or Bor alone, the proliferative potential of cells in combination group was significantly inhibited (p < 0.05), and apoptosis rate markedly increased (p < 0.05), cell cycle was arrested at G(1)-S phase, the mRNA expressive level of P21 and BAX increased, while the expression of BCL-2 decreased. Bortezomib 66-69 BCL2 associated X, apoptosis regulator Homo sapiens 309-312 20383943-7 2010 Besides, the NFkappaB pathway was not involved in bortezomib treatment in neuroblastoma CHP126 cells, bortezomib-driven apoptotic events were associated with promoting p21 and Bax expression and down-regulating Bcl-2 expression. Bortezomib 102-112 BCL2 associated X, apoptosis regulator Homo sapiens 176-179 21729550-7 2011 And RT-PCR showed, as compared with curcumin or bortezomib group, there was mRNA expression decrease of BCL-2, cyclin D1 but increase of BAX in combined group. Bortezomib 48-58 BCL2 associated X, apoptosis regulator Homo sapiens 137-140 20850924-2 2010 In the mutant TP53 MCL cells which are intrinsically resistant to bortezomib, the combination of Nutlin-3/bortezomib synergistically induced cytotoxicity through the mitochondrial apoptotic pathway mediated by transcription-independent upregulation of NOXA, sequestration of MCL-1, activation of BAX, BAK, caspase-9 and -3. Bortezomib 106-116 BCL2 associated X, apoptosis regulator Homo sapiens 296-299 19894220-7 2010 Our data showed that a proteasome inhibitor, bortezomib, increased Runx2 and Bax in osteosarcoma cells. Bortezomib 45-55 BCL2 associated X, apoptosis regulator Homo sapiens 77-80 21472287-5 2010 The combination of bortezomib and SAHA caused an increase in the ratio of bax/bcl-2 expression, inhibited the nuclear transportation of NF-kappaB, and down-regulated Akt expression and phosphorylation in HeLa cells. Bortezomib 19-29 BCL2 associated X, apoptosis regulator Homo sapiens 74-77 21459798-6 2011 All these changes lead to increased activation of Bax and Bak, loss of the mitochondrial membrane potential, cytochrome c release, caspase activation, and caspase-dependent apoptosis on treatment with bortezomib and TRAIL. Bortezomib 201-211 BCL2 associated X, apoptosis regulator Homo sapiens 50-53 19960346-8 2010 Velcade treatment resulted in G2M phase arrest, increased expression of cyclin-dependent kinase inhibitor p21 and pro-apoptotic protein Bax. Bortezomib 0-7 BCL2 associated X, apoptosis regulator Homo sapiens 136-139 20383943-9 2010 Above all, our data revealed that bortezomib triggered apoptosis by enhancing the caspase 3 activation and/or modulating the Bax/Bcl-2 balance, and also provided preliminary data for further researches of bortezomib on pediatric neuroblastoma. Bortezomib 34-44 BCL2 associated X, apoptosis regulator Homo sapiens 125-128 18445700-7 2008 Synergistic induction of apoptosis after exposure to LBH589 and bortezomib was partially mediated by Bax translocation from the cytosol to the mitochondria resulting from Bax conformational changes. Bortezomib 64-74 BCL2 associated X, apoptosis regulator Homo sapiens 101-104 18928586-0 2008 [Inducing-apoptosis effect of bortezomib on acute monocytic leukemia cell SHI-1 and its influence on expressions of Bcl2l12, Bcl-2 and Bax genes]. Bortezomib 30-40 BCL2 associated X, apoptosis regulator Homo sapiens 135-138 18928586-4 2008 RT-PCR was used to analyze the levels of Bcl2l12, Bcl-2 and bax mRNA in SHI-1 cells treated with bortezomib for 0, 6, 12 and 24 hours. Bortezomib 97-107 BCL2 associated X, apoptosis regulator Homo sapiens 60-63 19270531-2 2009 Concomitant or sequential exposure to non- or minimally toxic concentrations of bortezomib or other proteasome inhibitors and either HA14-1 or gossypol resulted in a striking increase in Bax/Bak conformational change/translocation, cytochrome c release, caspase activation and synergistic induction of apoptosis in both GC- and ABC-type cells. Bortezomib 80-90 BCL2 associated X, apoptosis regulator Homo sapiens 187-190 18445700-7 2008 Synergistic induction of apoptosis after exposure to LBH589 and bortezomib was partially mediated by Bax translocation from the cytosol to the mitochondria resulting from Bax conformational changes. Bortezomib 64-74 BCL2 associated X, apoptosis regulator Homo sapiens 171-174 18445700-8 2008 Bax translocation precedes cytochrome c release and apoptosis, and selective down-regulation of Bax using siRNA significantly mitigates the cytotoxicity of LBH589 and bortezomib. Bortezomib 167-177 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 18445700-8 2008 Bax translocation precedes cytochrome c release and apoptosis, and selective down-regulation of Bax using siRNA significantly mitigates the cytotoxicity of LBH589 and bortezomib. Bortezomib 167-177 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 18357392-9 2008 Bortezomib treatment increased the Bax protein expression. Bortezomib 0-10 BCL2 associated X, apoptosis regulator Homo sapiens 35-38 18357392-10 2008 Moreover, combination treatment of bortezomib plus docetaxel resulted in a dramatic increase in the Bax expression. Bortezomib 35-45 BCL2 associated X, apoptosis regulator Homo sapiens 100-103 18357392-14 2008 Further combination studies with other chemotherapeutic drugs, in particular docetaxel showing more tumor cell growth inhibition and apoptosis suggest that combining bortezomib with docetaxel might be more effective for displaying tumor cell growth inhibitory effects in gastric cancer cells through regulation of Bcl-2, Bax and p27 proteins in vitro. Bortezomib 166-176 BCL2 associated X, apoptosis regulator Homo sapiens 321-324 18160669-0 2008 Bortezomib blocks Bax degradation in malignant B cells during treatment with TRAIL. Bortezomib 0-10 BCL2 associated X, apoptosis regulator Homo sapiens 18-21 18160669-7 2008 In CLL cells, bortezomib induced Bax accumulation, translocation to mitochondria, conformational change, and oligomerization. Bortezomib 14-24 BCL2 associated X, apoptosis regulator Homo sapiens 33-36 18160669-8 2008 Accumulation and stabilization of Bax protein by bortezomib-sensitized malignant B cells to TRAIL-induced apoptosis. Bortezomib 49-59 BCL2 associated X, apoptosis regulator Homo sapiens 34-37 17308121-8 2007 In immunoglobulin-high cells, bortezomib increased the levels of proapoptotic Bax while reducing antiapoptotic Bcl-2. Bortezomib 30-40 BCL2 associated X, apoptosis regulator Homo sapiens 78-81 17912641-4 2007 We previously showed that proteasome inhibitors including MG132 and Bortezomib could induce apoptosis in a Bax- and caspase-dependent way. Bortezomib 68-78 BCL2 associated X, apoptosis regulator Homo sapiens 107-110 17545623-13 2007 Thus, in myeloma cells, the mechanistic basis for bortezomib sensitivity can be explained mainly by the model in which the sensitizer Noxa can displace Bim, a BH3-only activator, from Mcl-1, thus leading to Bax/Bak activation. Bortezomib 50-60 BCL2 associated X, apoptosis regulator Homo sapiens 207-210 17374988-8 2007 These data show that MG132 and bortezomib specifically sensitize leukemic cells to IDA through an increase in BIM and Bax pro-apoptotic Bcl-2 family proteins. Bortezomib 31-41 BCL2 associated X, apoptosis regulator Homo sapiens 118-121 16178003-3 2005 Proteasome inhibition with bortezomib has specifically promoted apoptosis of tumor cells through the stabilization of p53, p21, p27, Bax, and IkappaBalpha, resulting in nuclear factor kappaB inhibition. Bortezomib 27-37 BCL2 associated X, apoptosis regulator Homo sapiens 133-136 16424655-0 2006 Histone deacetylase inhibitor depsipeptide (FK228) induces apoptosis in leukemic cells by facilitating mitochondrial translocation of Bax, which is enhanced by the proteasome inhibitor bortezomib. Bortezomib 185-195 BCL2 associated X, apoptosis regulator Homo sapiens 134-137 16424655-6 2006 FK228-induced apoptosis and mitochondrial translocation of Bax were markedly enhanced by the proteasome inhibitor bortezomib. Bortezomib 114-124 BCL2 associated X, apoptosis regulator Homo sapiens 59-62 16424655-7 2006 The synergistic action of FK228 and bortezomib was at least partly mediated through conformational changes in Bax, which facilitate its translocation to the mitochondria. Bortezomib 36-46 BCL2 associated X, apoptosis regulator Homo sapiens 110-113 16166592-5 2006 Bortezomib induced phosphatidylserine exposure, mitochondrial depolarization, ROS generation, Bax and Bak conformational changes, and caspase activation. Bortezomib 0-10 BCL2 associated X, apoptosis regulator Homo sapiens 94-97 16382051-4 2005 Colon cancer cell lines lacking p53 or Bax were sensitized by bortezomib, suggesting that neither p53 nor Bax levels were crucial for sensitization. Bortezomib 62-72 BCL2 associated X, apoptosis regulator Homo sapiens 39-42 17018621-3 2006 Some therapeutic agents, such as bortezomib, not only induce proapoptotic Bcl-2 family members and active conformational changes in Bak and Bax but also are associated with undesirable effects, including accumulation of antiapoptotic proteins, such as Mcl-1. Bortezomib 33-43 BCL2 associated X, apoptosis regulator Homo sapiens 140-143 16219794-6 2006 Bortezomib at nanomolar concentrations inhibited constitutive activation of NF-kappaB and induced apoptosis of CTCL cells, with evidence of an upregulation of Bax expression. Bortezomib 0-10 BCL2 associated X, apoptosis regulator Homo sapiens 159-162 15929791-4 2005 Exposure to bortezomib has been shown to stabilize p21, p27, and p53, as well as the proapoptotic Bid and Bax proteins, caveolin-1, and inhibitor kappaB-alpha, which prevents activation of nuclear factor kappaB-induced cell survival pathways. Bortezomib 12-22 BCL2 associated X, apoptosis regulator Homo sapiens 106-109 15638966-3 2004 Bortezomib targets pathways relevant to tumor progression and therapy resistance and can directly modulate expression of cyclins, p27kip1, p53, nuclear factor-kB, Bcl-2, and Bax. Bortezomib 0-10 BCL2 associated X, apoptosis regulator Homo sapiens 174-177 15131062-9 2004 PS-341 not only inhibited nuclear localization of NF-kappaB but also activated the caspase cascade, increased p21 and Bax levels, and decreased Bcl-2 levels. Bortezomib 0-6 BCL2 associated X, apoptosis regulator Homo sapiens 118-121 14513055-6 2003 L-NAC also opposed bortezomib/HA14-1-mediated JNK activation, upregulation of p53 and Bax, and release of cytochrome c and Smac/DIABLO. Bortezomib 19-29 BCL2 associated X, apoptosis regulator Homo sapiens 86-89 14688479-0 2003 Differential apoptotic response to the proteasome inhibitor Bortezomib [VELCADE, PS-341] in Bax-deficient and p21-deficient colon cancer cells. Bortezomib 60-70 BCL2 associated X, apoptosis regulator Homo sapiens 92-95 14688479-0 2003 Differential apoptotic response to the proteasome inhibitor Bortezomib [VELCADE, PS-341] in Bax-deficient and p21-deficient colon cancer cells. Bortezomib 72-79 BCL2 associated X, apoptosis regulator Homo sapiens 92-95 14688479-0 2003 Differential apoptotic response to the proteasome inhibitor Bortezomib [VELCADE, PS-341] in Bax-deficient and p21-deficient colon cancer cells. Bortezomib 81-87 BCL2 associated X, apoptosis regulator Homo sapiens 92-95 14688479-6 2003 We demonstrated that bortezomib induced p53, and activated its downstream genes p21, PUMA and Bax in a p53-dependent fashion. Bortezomib 21-31 BCL2 associated X, apoptosis regulator Homo sapiens 94-97 14688479-8 2003 Surprisingly, we found that bortezomib-induced apoptosis was markedly enhanced in the p21-knockout cells, while significantly decreased in the BAX-knockout cells. Bortezomib 28-38 BCL2 associated X, apoptosis regulator Homo sapiens 143-146 33868466-10 2021 The mRNA expression levels of the proapoptotic genes Bcl-2-associated X protein (Bax) and Bak were significantly increased by bortezomib treatment and combination therapy with IR. Bortezomib 126-136 BCL2 associated X, apoptosis regulator Homo sapiens 53-79 12902978-0 2003 The proteasome inhibitor PS-341 overcomes TRAIL resistance in Bax and caspase 9-negative or Bcl-xL overexpressing cells. Bortezomib 25-31 BCL2 associated X, apoptosis regulator Homo sapiens 62-65 33868466-10 2021 The mRNA expression levels of the proapoptotic genes Bcl-2-associated X protein (Bax) and Bak were significantly increased by bortezomib treatment and combination therapy with IR. Bortezomib 126-136 BCL2 associated X, apoptosis regulator Homo sapiens 81-84 33376542-5 2021 Bortezomib treatment induced cell apoptosis in NB4 cells, as assessed by Annexin V/propidium iodide analysis, and the detection of cleaved caspase-3, cleaved poly(ADP-ribose) polymerase, Bax and Bcl-2 expression. Bortezomib 0-10 BCL2 associated X, apoptosis regulator Homo sapiens 187-190 33609728-14 2021 Finally, VO reverts bortezomib activity by counteracting ERK1/2, Bax, and caspase-3 activation. Bortezomib 20-30 BCL2 associated X, apoptosis regulator Homo sapiens 65-68 31322176-11 2019 Furthermore, the expression of HSP27 and Bcl-2 was significantly decreased, while the expression of Bax was increased by bortezomib and OGX-427 (P<0.05). Bortezomib 121-131 BCL2 associated X, apoptosis regulator Homo sapiens 100-103 32551032-11 2020 The western blot analysis revealed that nitroxoline or bortezomib treatment markedly diminished the levels of Bcl-2 and cyclin D1, and increased the levels of p21, Bax, cleaved PARP and cleaved caspase-3. Bortezomib 55-65 BCL2 associated X, apoptosis regulator Homo sapiens 164-167 31406244-7 2019 A combination screen reveals the proteasome inhibitor bortezomib (BTZ) and the histone deacetylase (HDAC) inhibitor vorinostat (SAHA) concertedly induce dramatic cell death in part through synergistic activation of BAX. Bortezomib 54-64 BCL2 associated X, apoptosis regulator Homo sapiens 215-218 31406244-7 2019 A combination screen reveals the proteasome inhibitor bortezomib (BTZ) and the histone deacetylase (HDAC) inhibitor vorinostat (SAHA) concertedly induce dramatic cell death in part through synergistic activation of BAX. Bortezomib 66-69 BCL2 associated X, apoptosis regulator Homo sapiens 215-218 32839432-6 2020 The combination with BZB additionally resulted in the accumulation of BOK, a BAX/BAK homologue, and of the BH3-only protein NOXA, which inhibits the anti-apoptotic protein MCL-1. Bortezomib 21-24 BCL2 associated X, apoptosis regulator Homo sapiens 77-80 32839432-8 2020 This synergistic mechanism of action was verified by CRISPR/Cas9 knock-out, showing that both BAX and NOXA are crucial for ABT-199/BZB-induced apoptosis. Bortezomib 131-134 BCL2 associated X, apoptosis regulator Homo sapiens 94-97