PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30583560-12 2018 SAHA appears to induce cell necroptosis in a p21-dependent manner, and RG7388 seems to induce apoptosis in a p21-independent manner, outlining differential mechanisms of cell death induction. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 45-48 22944197-9 2013 Vorinostat induced G2/M arrest, an increase in the sub-G1 fraction, up-regulation of p21, and down-regulation of TS in all UCC. Vorinostat 0-10 H3 histone pseudogene 16 Homo sapiens 85-88 30583560-7 2018 Induction of cell cycle arrest by SAHA in cancer cells was evidenced by elevated p21 protein levels. Vorinostat 34-38 H3 histone pseudogene 16 Homo sapiens 81-84 26410576-6 2015 Furthermore, vorinostat-NPs have similar effectiveness in the suppression or expression of histone deacetylase, mutant type p53, p21, and PARP/cleaved caspase-3. Vorinostat 13-23 H3 histone pseudogene 16 Homo sapiens 129-132 29290529-8 2018 RESULTS: Treatment with SAHA inhibited the proliferation of SK-Mel-5 cells, enhanced the phosphorylation of R-Smad, and up-regulated p21 protein. Vorinostat 24-28 H3 histone pseudogene 16 Homo sapiens 133-136 30091530-5 2018 SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 93-96 27911270-3 2017 The treatment with SAHA increased the expression of acetyl-histones 3 and 4, which were recruited to the promoters of p21, p27, Cyclin D1, c-myc and Nanog to down-regulate their transcriptional levels. Vorinostat 19-23 H3 histone pseudogene 16 Homo sapiens 118-121 26314218-13 2016 In addition, in vitro exposure of RRCL to vorinostat resulted in an increase in p21 and acetylation of histone H3 leading to G1 cell cycle arrest. Vorinostat 42-52 H3 histone pseudogene 16 Homo sapiens 80-83 23299388-6 2013 Induction of acetyl-H3, acetyl-H4 and p21 by vorinostat were transient and rapidly reversed within 12 h of drug removal. Vorinostat 45-55 H3 histone pseudogene 16 Homo sapiens 38-41 26713523-7 2015 Treatment with 2.5mumol/L SAHA significantly up-regulated the expression of p21 protein in 48 h, while the protein expression was reduced in combined treatment with 5mumol/L lovastatin. Vorinostat 26-30 H3 histone pseudogene 16 Homo sapiens 76-79 26713523-8 2015 CONCLUSION: Statins can synergize the anti-tumor effect of SAHA in human NSCLC cells through a p21-dependent way. Vorinostat 59-63 H3 histone pseudogene 16 Homo sapiens 95-98 26038719-12 2015 SAHA alone showed increased expression of p21, while ATO alone and in combination with SAHA showed no significant change. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 42-45 26101701-6 2015 SAHA and GDC-0449 cooperatively enhanced G0/G1 cell cycle arrest which was associated with up-regulation of p21(waf). Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 108-111 24236158-6 2013 In contrast, SAHA increased expression of Caspase-3, p21 and p53 mRNA, and upregulated acetyl-Histones H3 and H4, Caspase-8, and p53 proteins. Vorinostat 13-17 H3 histone pseudogene 16 Homo sapiens 53-56 26713523-4 2015 The expression of cleaved poly-ADP-ribose polymerase(cleaved-PARP) and p21 protein was analyzed by Western-blotting when A549 cells were challenged with 2.5mumol/L SAHA and 5mumol/L lovastatin. Vorinostat 164-168 H3 histone pseudogene 16 Homo sapiens 71-74 26050346-13 2015 CONCLUSION: SAHA promotes SiHa apoptosis in chemotherapy through up-regulation of mRNA and protein of p21 and Bax which leads to cell cycle arrest in G0/G1 phase. Vorinostat 12-16 H3 histone pseudogene 16 Homo sapiens 102-105 25116350-0 2014 Up-regulation of P21 inhibits TRAIL-mediated extrinsic apoptosis, contributing resistance to SAHA in acute myeloid leukemia cells. Vorinostat 93-97 H3 histone pseudogene 16 Homo sapiens 17-20 25116350-2 2014 In this study we examined the effect of altered p21 expression on the sensitivity of acute myeloid leukemia cells in response to HDAC inhibitor SAHA treatment and investigated the underlying mechanism. Vorinostat 144-148 H3 histone pseudogene 16 Homo sapiens 48-51 25116350-8 2014 Enforced expression of p21 in HL60 cells reduced sensitivity to SAHA and blocked TRAIL-mediated apoptosis. Vorinostat 64-68 H3 histone pseudogene 16 Homo sapiens 23-26 25116350-9 2014 Conversely, p21 silencing in NB4 cells enhanced SAHA-mediated apoptosis and lethality. Vorinostat 48-52 H3 histone pseudogene 16 Homo sapiens 12-15 25116350-10 2014 Finally, we found that combined treatment with SAHA and rapamycin down-regulated p21 and enhanced apoptosis in AML cells. Vorinostat 47-51 H3 histone pseudogene 16 Homo sapiens 81-84 25116350-11 2014 CONCLUSION: We conclude that up-regulated p21 expression mediates resistance to SAHA via inhibition of TRAIL apoptotic pathway. Vorinostat 80-84 H3 histone pseudogene 16 Homo sapiens 42-45 25116350-12 2014 P21 may serve as a candidate biomarker to predict responsiveness or resistance to SAHA-based therapy in AML patients. Vorinostat 82-86 H3 histone pseudogene 16 Homo sapiens 0-3 25116350-13 2014 In addition, rapamycin may be an effective agent to override p21-mediated resistance to SAHA in AML patients. Vorinostat 88-92 H3 histone pseudogene 16 Homo sapiens 61-64 23903894-1 2013 INTRODUCTION: Vorinostat is a small molecule inhibitor of class I and II histone deacetylase enzymes which alters the expression of target genes including the cell cycle gene p21, leading to cell cycle arrest and apoptosis. Vorinostat 14-24 H3 histone pseudogene 16 Homo sapiens 175-178 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. Vorinostat 107-117 H3 histone pseudogene 16 Homo sapiens 0-3 23903894-9 2013 The ChIP assay demonstrated a protein-DNA interaction, in this case interaction of Nur77, HSP70 and p21 with acetylated histone H3, at baseline and at day 9 after treatment with vorinostat in tissue biopsies in most patients. Vorinostat 178-188 H3 histone pseudogene 16 Homo sapiens 100-103 23903894-10 2013 CONCLUSION: Vorinostat inhibits Nur77 expression, which in turn may decrease p21 and AKT expression in PBMCs. Vorinostat 12-22 H3 histone pseudogene 16 Homo sapiens 77-80 22484732-3 2012 Vorinostat significantly reduced BrdU incorporation in MDA-MB-231 and MCF-7 cells, which was associated with increased p27 and p21 protein levels without concomitant induction of p27 mRNA. Vorinostat 0-10 H3 histone pseudogene 16 Homo sapiens 151-154 23515411-11 2013 Ex vivo exposure of leukemia cells to plasma obtained from patients after alvocidib treatment blocked vorinostat-mediated p21(CIP1) induction and downregulated Mcl-1 and p-RNA Pol II for some specimens, although parallel in vivo bone marrow responses were infrequent. Vorinostat 102-112 H3 histone pseudogene 16 Homo sapiens 122-125 22484732-0 2012 Vorinostat enhances protein stability of p27 and p21 through negative regulation of Skp2 and Cks1 in human breast cancer cells. Vorinostat 0-10 H3 histone pseudogene 16 Homo sapiens 49-52 22711276-7 2012 Exposure to valproic acid and suberoylanilide hydroxamic acid was associated with increased levels of p21 and FOXO3 and reduced expression of survivin. Vorinostat 30-61 H3 histone pseudogene 16 Homo sapiens 102-105 22484732-4 2012 Vorinostat-induced accumulation of p27 and p21 proteins was inversely correlated with the mRNA and protein levels of Skp2 and Cks1. Vorinostat 0-10 H3 histone pseudogene 16 Homo sapiens 43-46 22484732-5 2012 Cycloheximide chase analysis revealed that vorinostat increased the half-life of p27 and p21 proteins. Vorinostat 55-65 H3 histone pseudogene 16 Homo sapiens 101-104 22484732-6 2012 The accumulation of p27 and p21 proteins was attenuated by forced expression of Skp2 and Cks1, which conferred resistance to the vorinostat-induced S-phase reduction. Vorinostat 153-163 H3 histone pseudogene 16 Homo sapiens 40-43 22484732-7 2012 These results suggest that vorinostat-induced growth arrest may be in part due to the enhanced protein stability of p27 and p21 through the downregulation of Skp2 and Cks1. Vorinostat 27-37 H3 histone pseudogene 16 Homo sapiens 136-139 22075951-6 2012 Suppression of p21 induction by p21 siRNA reversed the suppressive effect of vorinostat on the replication of CRAd, but still failed to reverse the antagonistic interaction. Vorinostat 77-87 H3 histone pseudogene 16 Homo sapiens 32-35 22075951-6 2012 Suppression of p21 induction by p21 siRNA reversed the suppressive effect of vorinostat on the replication of CRAd, but still failed to reverse the antagonistic interaction. Vorinostat 77-87 H3 histone pseudogene 16 Homo sapiens 15-18 21205092-7 2011 Furthermore, vorinostat-induced RUNX3 significantly enhanced p21 expression and growth inhibition of Mz-ChA-2 cells through restoration of TGF-beta signaling. Vorinostat 13-23 H3 histone pseudogene 16 Homo sapiens 61-64 21889949-7 2011 At the doses used, ATO did not interfere with cell cycle progression, but SAHA induced p21 expression and led to G1 arrest. Vorinostat 74-78 H3 histone pseudogene 16 Homo sapiens 87-90 21933400-12 2011 However, p21 was significantly increased by SAHA and combination treatment as compared to HIT only in the two sarcoma cell lines--again in contrast to the osteoblast cell line. Vorinostat 44-48 H3 histone pseudogene 16 Homo sapiens 9-12 21933400-13 2011 Changes in the repair kinetics of DSB p53-independent apoptosis with p21 involvement may be part of the underlying mechanisms for radio-sensitization by SAHA. Vorinostat 153-157 H3 histone pseudogene 16 Homo sapiens 69-72 18541724-3 2008 In this study, we report that the HDAC inhibitor vorinostat induced p21 expression and decreased Bcl-xL levels causing cell-cycle arrest and apoptosis. Vorinostat 49-59 H3 histone pseudogene 16 Homo sapiens 68-71 20665144-8 2010 SAHA treatment added to ad-p63/p73 gene delivery caused an increase in p21 expression and cleaved poly-ADP ribose polymerase. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 71-74 19440035-7 2009 Treatment of MCL cells with vorinostat or 17-DMAG was associated with the inductionof p21 and p27, as well as with depletion of c-Myc, c-RAF, AKT and CDK4. Vorinostat 28-38 H3 histone pseudogene 16 Homo sapiens 86-89 19553104-4 2009 At a low concentration SAHA decreases Ki-67 and cyclin A positive cells and increases p21 positive cells in the outer layer while it induces a ROS-dependent apoptosis in the central zone of the spheroid. Vorinostat 23-27 H3 histone pseudogene 16 Homo sapiens 86-89 19553104-5 2009 Coimmunostaining of p21 and apoptotic cells confirms that SAHA effects are different depending on the position of the cells within the spheroid. Vorinostat 58-62 H3 histone pseudogene 16 Homo sapiens 20-23 19157955-5 2009 Western blot analyses demonstrated that the expression of p21 protein was remarkably augmented and hyperacetylation of p53 was induced after SAHA treatment. Vorinostat 141-145 H3 histone pseudogene 16 Homo sapiens 58-61 16343270-9 2006 SAHA lead to an upregulation of p21 in all cell lines and an upregulation of p27 in JeKo-1 and Granta-519 cells, while expression of p27 in Hbl-2 was not altered. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 32-35 17200334-6 2007 This arrest was dependent, in part, on induction of p21 by SAHA, as p21 was not induced in PANC-1 cells, and knockdown of p21 using small interfering RNA oligonucleotides nearly completely suppressed the effects of SAHA on cell cycle arrest in COLO-357 and partly attenuated the effects of SAHA in BxPC-3. Vorinostat 59-63 H3 histone pseudogene 16 Homo sapiens 52-55 17200334-6 2007 This arrest was dependent, in part, on induction of p21 by SAHA, as p21 was not induced in PANC-1 cells, and knockdown of p21 using small interfering RNA oligonucleotides nearly completely suppressed the effects of SAHA on cell cycle arrest in COLO-357 and partly attenuated the effects of SAHA in BxPC-3. Vorinostat 59-63 H3 histone pseudogene 16 Homo sapiens 68-71 17200334-6 2007 This arrest was dependent, in part, on induction of p21 by SAHA, as p21 was not induced in PANC-1 cells, and knockdown of p21 using small interfering RNA oligonucleotides nearly completely suppressed the effects of SAHA on cell cycle arrest in COLO-357 and partly attenuated the effects of SAHA in BxPC-3. Vorinostat 59-63 H3 histone pseudogene 16 Homo sapiens 68-71 17200334-6 2007 This arrest was dependent, in part, on induction of p21 by SAHA, as p21 was not induced in PANC-1 cells, and knockdown of p21 using small interfering RNA oligonucleotides nearly completely suppressed the effects of SAHA on cell cycle arrest in COLO-357 and partly attenuated the effects of SAHA in BxPC-3. Vorinostat 215-219 H3 histone pseudogene 16 Homo sapiens 52-55 17200334-6 2007 This arrest was dependent, in part, on induction of p21 by SAHA, as p21 was not induced in PANC-1 cells, and knockdown of p21 using small interfering RNA oligonucleotides nearly completely suppressed the effects of SAHA on cell cycle arrest in COLO-357 and partly attenuated the effects of SAHA in BxPC-3. Vorinostat 215-219 H3 histone pseudogene 16 Homo sapiens 52-55 17200334-10 2007 Moreover, analysis of p21 distribution in COLO-357 cells revealed that SAHA induced the cytoplasmic localization of both p21 and phospho-p21. Vorinostat 71-75 H3 histone pseudogene 16 Homo sapiens 22-25 17200334-10 2007 Moreover, analysis of p21 distribution in COLO-357 cells revealed that SAHA induced the cytoplasmic localization of both p21 and phospho-p21. Vorinostat 71-75 H3 histone pseudogene 16 Homo sapiens 121-124 17200334-10 2007 Moreover, analysis of p21 distribution in COLO-357 cells revealed that SAHA induced the cytoplasmic localization of both p21 and phospho-p21. Vorinostat 71-75 H3 histone pseudogene 16 Homo sapiens 121-124 17200334-11 2007 CONCLUSIONS: These data indicate that SAHA exerts proapoptotic effects in pancreatic cancer cells, in part, by up-regulating p21 and sequestering it in the cytoplasm, raising the possibility that SAHA may have therapeutic potential in the treatment of pancreatic cancer. Vorinostat 38-42 H3 histone pseudogene 16 Homo sapiens 125-128 15661398-8 2005 SAHA downregulated cyclin D1 and D2, and upregulated p53, p21, and p27. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 58-61 15897598-4 2005 In these models, both SAHA and m-carboxycinnamic acid bis-hydroxamide induced growth arrest and caspase-mediated apoptosis and increased p21 protein levels, retinoblastoma hypophosphorylation, BH3-interacting domain death agonist cleavage, Bax up-regulation, down-regulation of Bcl-2, A1, and Bcl-x(L) expression, and cleavage of poly(ADP-ribose) polymerase and caspase-8, -9, -3, -7, and -2. Vorinostat 22-26 H3 histone pseudogene 16 Homo sapiens 137-140 15661398-9 2005 Chromatin immunoprecipitation analysis revealed a remarkable increase in the level of acetylated histones associated with the p21 promoter after SAHA treatment. Vorinostat 145-149 H3 histone pseudogene 16 Homo sapiens 126-129 14679005-5 2003 Coadministration of 17-AAG blocked SAHA-mediated induction of the cyclin-dependent kinase inhibitor p21(CIP1) and resulted in reduced expression of p27(KIP1) and p34(cdc2). Vorinostat 35-39 H3 histone pseudogene 16 Homo sapiens 100-103 14679005-7 2003 Enforced expression of doxycycline-inducible p21(CIP1) or constitutively active MEK1 significantly diminished 17-AAG/SAHA-mediated lethality, indicating that interference with ERK activation and p21(CIP1) induction play important functional roles in the lethal effects of this regimen. Vorinostat 117-121 H3 histone pseudogene 16 Homo sapiens 45-48 12531799-4 2003 SAHA induced apoptosis in all tumor cells tested, with increased p21 and p53 protein levels and dephosphorylation of Rb. Vorinostat 0-4 H3 histone pseudogene 16 Homo sapiens 65-68 12446442-1 2003 Here we demonstrate that treatment with SAHA (suberoylanilide hydroxamic acid), a known inhibitor of histone deacetylases (HDACs), alone induced p21 and/or p27 expressions but decreased the mRNA and protein levels of Bcr-Abl, which was associated with apoptosis of Bcr-Abl-expressing K562 and LAMA-84 cells. Vorinostat 40-44 H3 histone pseudogene 16 Homo sapiens 145-148 12446442-1 2003 Here we demonstrate that treatment with SAHA (suberoylanilide hydroxamic acid), a known inhibitor of histone deacetylases (HDACs), alone induced p21 and/or p27 expressions but decreased the mRNA and protein levels of Bcr-Abl, which was associated with apoptosis of Bcr-Abl-expressing K562 and LAMA-84 cells. Vorinostat 46-77 H3 histone pseudogene 16 Homo sapiens 145-148