PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 H3 histone pseudogene 16 Homo sapiens 159-162 28055975-8 2017 Transient p21 knockdown alleviates BTZ-induced senescence inhibition, G2-M cell cycle blockade, and mitotic catastrophe. Bortezomib 35-38 H3 histone pseudogene 16 Homo sapiens 10-13 28161489-9 2017 Consistent with FOXO1 dephosphorylation/activation, p21 mRNA expression is increased by Bortezomib in a MKP-3-dependent way. Bortezomib 88-98 H3 histone pseudogene 16 Homo sapiens 52-55 28161489-11 2017 It is concluded that in vGPCR cells, Bortezomib decreases ERK1/2 and FOXO1 phosphorylation through MKP-3 accumulation, leading ERK1/2 deactivation and FOXO1 activation respectively and, consequently, to cell proliferation inhibition, p21 induction and VEGF repression. Bortezomib 37-47 H3 histone pseudogene 16 Homo sapiens 234-237 28055975-7 2017 BTZ stabilized p21, CDC2, and cyclin B in RRCL and in primary tumor cells. Bortezomib 0-3 H3 histone pseudogene 16 Homo sapiens 15-18 28055975-9 2017 Our data suggest that BTZ can induce apoptosis or mitotic catastrophe and that p21 has a pivotal role in BTZ activity against RRCL. Bortezomib 105-108 H3 histone pseudogene 16 Homo sapiens 79-82 26025442-7 2015 RESULTS: We report that Bz-surviving MM cells in vitro and in vivo enter quiescence characterized by p21(CIP1) upregulation. Bortezomib 24-26 H3 histone pseudogene 16 Homo sapiens 101-104 26378933-7 2015 Corroborating the clinical outcome of the patients, our data provides a potential explanation regarding the poor response of MM patients with del(8)(p21) to bortezomib treatment. Bortezomib 157-167 H3 histone pseudogene 16 Homo sapiens 149-152 26378933-2 2015 In this study, we aimed to identify the immunological and molecular consequences of del(8)(p21) with regards to treatment response and bortezomib resistance. Bortezomib 135-145 H3 histone pseudogene 16 Homo sapiens 91-94 26378933-3 2015 In patients receiving bortezomib as a single first line agent without any high-dose therapy, we have observed that patients with del(8)(p21) responded poorly to bortezomib with 50% showing no response while patients without the deletion had a response rate of 90%. Bortezomib 22-32 H3 histone pseudogene 16 Homo sapiens 136-139 26378933-3 2015 In patients receiving bortezomib as a single first line agent without any high-dose therapy, we have observed that patients with del(8)(p21) responded poorly to bortezomib with 50% showing no response while patients without the deletion had a response rate of 90%. Bortezomib 161-171 H3 histone pseudogene 16 Homo sapiens 136-139 26378933-4 2015 In vitro analysis revealed a higher resistance to bortezomib possibly due to an altered gene expression profile caused by del(8)(p21) including genes such as TRAIL-R4, CCDC25, RHOBTB2, PTK2B, SCARA3, MYC, BCL2 and TP53. Bortezomib 50-60 H3 histone pseudogene 16 Homo sapiens 129-132 26025442-14 2015 CONCLUSIONS: We conclude that Bz-surviving MM cells display a GRP78(HIGH)/p21(HIGH)/CDK6(LOW)/P-Rb(LOW) profile, and these markers may identify quiescent MM cells capable of fueling recurrences. Bortezomib 30-32 H3 histone pseudogene 16 Homo sapiens 74-77 19608275-7 2010 The enhanced cytotoxicity of ATO+bortezomib was associated with augmented STAT3 inhibition and JNK activation, up-regulation of Bim, p21, p27, p53 as well as down-regulation of Bcl-2. Bortezomib 33-43 H3 histone pseudogene 16 Homo sapiens 133-136 24380881-4 2014 BTZ-treated HTLA-230 cells down-regulated p53 and up-regulated p21, favoring cell survival. Bortezomib 0-3 H3 histone pseudogene 16 Homo sapiens 63-66 24380881-5 2014 The inhibition of HO-1 activity obtained by Zinc (II) protoprophyrin IX (ZnPPIX) was able to significantly increase the pro-apoptotic effect of BTZ in a p53- and p21-independent way. Bortezomib 144-147 H3 histone pseudogene 16 Homo sapiens 162-165 24485799-4 2014 In this study, we investigate whether combined treatment with romidepsin and bortezomib would induce apoptosis in A549 NSCLC cells by activating cell cycle arrest, enhanced generation of p21 and p53, down-regulation of matrix metalloproteinases (MMPs) 2,9 also altering the acetylation status of histone proteins. Bortezomib 77-87 H3 histone pseudogene 16 Homo sapiens 187-190 24485799-5 2014 Our data show that combination of romidepsin and bortezomib caused cell cycle arrest at Sub G0-G1 transition, up-regulation of cell cycle protein p21 and tumour suppressor protein p53. Bortezomib 49-59 H3 histone pseudogene 16 Homo sapiens 146-149 23716467-0 2013 Bortezomib induces apoptosis of endometrial cancer cells through microRNA-17-5p by targeting p21. Bortezomib 0-10 H3 histone pseudogene 16 Homo sapiens 93-96 23716467-7 2013 The transfection of miR-17-5p mimics or siRNA-p21 reversed the effect of bortezomib on HTB-111 and Ishikawa cells, indicating that miR-17-5p may mediate the function of bortezomib by targeting p21 in endometrial cancer cells. Bortezomib 73-83 H3 histone pseudogene 16 Homo sapiens 46-49 23716467-7 2013 The transfection of miR-17-5p mimics or siRNA-p21 reversed the effect of bortezomib on HTB-111 and Ishikawa cells, indicating that miR-17-5p may mediate the function of bortezomib by targeting p21 in endometrial cancer cells. Bortezomib 73-83 H3 histone pseudogene 16 Homo sapiens 193-196 23716467-7 2013 The transfection of miR-17-5p mimics or siRNA-p21 reversed the effect of bortezomib on HTB-111 and Ishikawa cells, indicating that miR-17-5p may mediate the function of bortezomib by targeting p21 in endometrial cancer cells. Bortezomib 169-179 H3 histone pseudogene 16 Homo sapiens 46-49 23716467-7 2013 The transfection of miR-17-5p mimics or siRNA-p21 reversed the effect of bortezomib on HTB-111 and Ishikawa cells, indicating that miR-17-5p may mediate the function of bortezomib by targeting p21 in endometrial cancer cells. Bortezomib 169-179 H3 histone pseudogene 16 Homo sapiens 193-196 23903894-8 2013 p21, a downstream target of Nur77, was significantly decreased on day 9, 2 and 6 h after administration of vorinostat and bortezomib, 0.67 (0.41-1.03) (p < 0.01); 0.44 (0.25-1.3) (p < 0.01), respectively. Bortezomib 122-132 H3 histone pseudogene 16 Homo sapiens 0-3 22559167-7 2012 The effects of rapamycin and/or bortezomib on the mRNA expression levels of p53, p27, p21 and Bcl-2 family in HCCLM3 cells were evaluated by RT-PCR. Bortezomib 32-42 H3 histone pseudogene 16 Homo sapiens 86-89 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 H3 histone pseudogene 16 Homo sapiens 301-304 22087283-9 2011 The combination of bortezomib and ATRA triggered increased differentiation through the activation of proteins, including RARalpha, RARbeta, RARgamma, p-JNK and p21, compared with ATRA treatment alone. Bortezomib 19-29 H3 histone pseudogene 16 Homo sapiens 160-163 20397022-9 2010 Cell cycle inhibitors p21 and p27 are induced in the three cell lines by bortezomib and the combination treatment. Bortezomib 73-83 H3 histone pseudogene 16 Homo sapiens 22-25 24263099-6 2013 Importantly, Bortezomib inhibits G2/M transition by inhibiting proteasomal degradation of cell cycle regulatory proteins such as p21, thereby preventing cells to enter mitosis, the cell cycle phase in which they are most vulnerable to antitubulin chemotherapeutics. Bortezomib 13-23 H3 histone pseudogene 16 Homo sapiens 129-132 23449448-3 2013 In this study, we show that bortezomib induced apoptosis, which was demonstrated by the downregulation of antiapoptotic molecules (Bcl-2, Bcl-XL, p-Bad, and p-AKT) and the upregulation of proapoptotic proteins (p21, p27, and cleaved-Bid) in ovarian cancer cell lines. Bortezomib 28-38 H3 histone pseudogene 16 Homo sapiens 211-214 23064281-7 2013 In addition, sequential or concomitant treatment of bortezomib and cisplatin stimulated the expression of p53, hScrib and p21 and the stimulation was markedly influenced by the order of drugs in HeLa cells. Bortezomib 52-62 H3 histone pseudogene 16 Homo sapiens 134-137 22231280-5 2012 Here we show that single-agent bortezomib treatment of MCL cell lines leads to G2/M arrest and induction of apoptosis accompanied by downregulation of EIF4E and CCND1 mRNA but upregulation of p15(INK4B) and p21 mRNA. Bortezomib 31-41 H3 histone pseudogene 16 Homo sapiens 207-210 22324515-7 2012 Bad, p53, p21 and p27 were downregulated by neuropeptides in PC-3, and these effects were reversed with the addition of bortezomib. Bortezomib 120-130 H3 histone pseudogene 16 Homo sapiens 10-13 21429402-9 2011 BTZ alone significantly increased the proportion of cells in G(2)/M phase (P < 0.01) in a dose-dependent manner and up-regulated the expression level of P21. Bortezomib 0-3 H3 histone pseudogene 16 Homo sapiens 156-159 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 H3 histone pseudogene 16 Homo sapiens 168-171 15662128-5 2005 Apoptosis induced by Bortezomib was associated with inhibition of the classical and alternative NF-kappaB pathways, upregulation of p53, p21 and p27 and activation of caspase cascade. Bortezomib 21-31 H3 histone pseudogene 16 Homo sapiens 137-140 19661301-6 2009 Cytotoxicity in cell lines that differed in intrinsic sensitivity to bortezomib correlated with sustained inhibition of proteasome activity, survivin expression and induction of p21 expression. Bortezomib 69-79 H3 histone pseudogene 16 Homo sapiens 178-181 18445700-5 2008 LBH589 or bortezomib alone increased expression of the cell cycle regulators p21 and p27. Bortezomib 10-20 H3 histone pseudogene 16 Homo sapiens 77-80 18223318-5 2008 Bortezomib-induced apoptosis was associated with activation of caspase 3, cleavage of PARP and induction of p27 and p21 expression. Bortezomib 0-10 H3 histone pseudogene 16 Homo sapiens 116-119 17762396-5 2007 Bortezomib produced significant growth inhibition in these cells (mean IC50 values: 1.26, 9.44 and 8.63 micromol/l, respectively) and was also observed to decrease the activity of the extracellular signal-regulated kinase 1/2 and Akt signal pathways, increasing the accumulation of p21. Bortezomib 0-10 H3 histone pseudogene 16 Homo sapiens 282-285 16849420-8 2006 Bortezomib inhibited NF-kappaB activity; increased p53, p21, and jun expression; and induced caspase-dependent apoptosis. Bortezomib 0-10 H3 histone pseudogene 16 Homo sapiens 56-59 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 H3 histone pseudogene 16 Homo sapiens 123-126 15464472-13 2004 Combined gemcitabine and bortezomib enhanced p21 and p53 expression and induced S-phase and G2/M cell-cycle arrests, respectively. Bortezomib 25-35 H3 histone pseudogene 16 Homo sapiens 45-48 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 H3 histone pseudogene 16 Homo sapiens 80-83 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 H3 histone pseudogene 16 Homo sapiens 110-113 15052205-11 2004 The proteins p21 and p53 were stabilized after treatment with bortezomib, correlating with a G(2)/M cell-cycle arrest. Bortezomib 62-72 H3 histone pseudogene 16 Homo sapiens 13-16 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 H3 histone pseudogene 16 Homo sapiens 86-89 12738242-4 2003 Bortezomib also appeared to increase the stabilization of p21 and p27, as well as transcription factor p53. Bortezomib 0-10 H3 histone pseudogene 16 Homo sapiens 58-61 11740818-6 2001 PS-341 inhibits p44/42 mitogen-activated protein kinase (MAPK) growth signaling triggered by IL-6 and induces apoptosis, despite induction of p21 and p27, in p53 wild-type and p53 mutant MM cells. Bortezomib 0-6 H3 histone pseudogene 16 Homo sapiens 142-145 11306489-3 2001 In this study, we demonstrate that the proteasome inhibitor PS-341 directly inhibits proliferation and induces apoptosis of human MM cell lines and freshly isolated patient MM cells; inhibits mitogen-activated protein kinase growth signaling in MM cells; induces apoptosis despite induction of p21 and p27 in both p53 wild-type and p53 mutant MM cells; overcomes drug resistance; adds to the anti-MM activity of dexamethasone; and overcomes the resistance to apoptosis in MM cells conferred by interleukin-6. Bortezomib 60-66 H3 histone pseudogene 16 Homo sapiens 294-297