PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17919121-1 2008 Polyamines are required for maintenance of intestinal epithelial integrity, and a decrease in cellular polyamines increases the cytoplasmic levels of RNA-binding protein HuR stabilizing p53 and nucleophosmin mRNAs, thus inhibiting IEC (intestinal epithelial cell) proliferation. Polyamines 103-113 tumor protein p53 Homo sapiens 186-189 19584241-0 2009 Inhibition of S-adenosylmethionine decarboxylase by inhibitor SAM486A connects polyamine metabolism with p53-Mdm2-Akt/protein kinase B regulation and apoptosis in neuroblastoma. Polyamines 79-88 tumor protein p53 Homo sapiens 105-108 19584241-8 2009 The results presented in this study highlight the importance of PA homeostasis and provide a direct link between PA metabolism and apoptotic cell signaling pathways in p53 wild-type NB cells. Polyamines 113-115 tumor protein p53 Homo sapiens 168-171 15180186-10 2004 Polyamine biosynthesis was significantly higher in cancers showing K-ras mutation, either with or without p53 mutation [K-ras(+)/p53(-) and K-ras(+)/p53(+)], compared to samples with K-ras wild type [K-ras(-)/p53(-) and K-ras(-)/p53(+)]. Polyamines 0-9 tumor protein p53 Homo sapiens 129-132 17804813-2 2007 Recently, polyamines were shown to regulate the subcellular localization of the RNA-binding protein HuR, which stabilizes its target transcripts such as nucleophosmin and p53 mRNAs. Polyamines 10-20 tumor protein p53 Homo sapiens 171-174 17442733-10 2007 These results indicate that NDRG1 is one of the direct mediators of induced p53 following polyamine depletion and that p53-dependent NDRG1 expression plays a critical role in the negative control of IEC proliferation. Polyamines 90-99 tumor protein p53 Homo sapiens 76-79 16131835-0 2005 Role of p53/p21(Waf1/Cip1) in the regulation of polyamine analogue-induced growth inhibition and cell death in human breast cancer cells. Polyamines 48-57 tumor protein p53 Homo sapiens 8-11 16131835-7 2005 Stable transfection of small interfering RNA (siRNA) targeting p53 blocked the expression of p21 induced by the polyamine analogues and significantly reduced polyamine analogue-induced growth inhibition and apoptosis, suggesting that polyamine analogue-induced p21 expression occurs through p53-dependent mechanisms. Polyamines 112-121 tumor protein p53 Homo sapiens 63-66 16131835-7 2005 Stable transfection of small interfering RNA (siRNA) targeting p53 blocked the expression of p21 induced by the polyamine analogues and significantly reduced polyamine analogue-induced growth inhibition and apoptosis, suggesting that polyamine analogue-induced p21 expression occurs through p53-dependent mechanisms. Polyamines 158-167 tumor protein p53 Homo sapiens 63-66 16131835-7 2005 Stable transfection of small interfering RNA (siRNA) targeting p53 blocked the expression of p21 induced by the polyamine analogues and significantly reduced polyamine analogue-induced growth inhibition and apoptosis, suggesting that polyamine analogue-induced p21 expression occurs through p53-dependent mechanisms. Polyamines 158-167 tumor protein p53 Homo sapiens 63-66 16131835-9 2005 Expression of p53 siRNA reversed only BENSpm-modulated the cell cycle arrest, suggesting that regulation of cell cycle arrest by p53/p21 induced by polyamine analogues occurs through agent-specific mechanisms. Polyamines 148-157 tumor protein p53 Homo sapiens 14-17 16131835-9 2005 Expression of p53 siRNA reversed only BENSpm-modulated the cell cycle arrest, suggesting that regulation of cell cycle arrest by p53/p21 induced by polyamine analogues occurs through agent-specific mechanisms. Polyamines 148-157 tumor protein p53 Homo sapiens 129-132 16131835-10 2005 Understanding the mechanism of p53-mediated cellular responses to polyamine analogue may help to improve the therapeutic efficacy of polyamine analogues in human breast cancer. Polyamines 66-75 tumor protein p53 Homo sapiens 31-34 16131835-10 2005 Understanding the mechanism of p53-mediated cellular responses to polyamine analogue may help to improve the therapeutic efficacy of polyamine analogues in human breast cancer. Polyamines 133-142 tumor protein p53 Homo sapiens 31-34 15546879-4 2005 Our results showed that simultaneous 5-FU and DENSPM, a spermine analogue, synergistically increased transcript levels of the polyamine catabolism enzyme spermidine/spermine N1-acetyltransferase, depleted spermine and spermidine, increased acetylated spermidine, and produced synergistic tumor cell apoptosis in both p53 wild-type and p53-null variants. Polyamines 126-135 tumor protein p53 Homo sapiens 317-320 15546879-4 2005 Our results showed that simultaneous 5-FU and DENSPM, a spermine analogue, synergistically increased transcript levels of the polyamine catabolism enzyme spermidine/spermine N1-acetyltransferase, depleted spermine and spermidine, increased acetylated spermidine, and produced synergistic tumor cell apoptosis in both p53 wild-type and p53-null variants. Polyamines 126-135 tumor protein p53 Homo sapiens 335-338 17442733-0 2007 p53-dependent NDRG1 expression induces inhibition of intestinal epithelial cell proliferation but not apoptosis after polyamine depletion. Polyamines 118-127 tumor protein p53 Homo sapiens 0-3 17442733-2 2007 Our previous studies have shown that polyamine depletion stabilizes p53, resulting in inhibition of intestinal epithelial cell (IEC) proliferation, but the exact downstream targets of induced p53 are still unclear. Polyamines 37-46 tumor protein p53 Homo sapiens 68-71 17442733-4 2007 The current study tests the hypothesis that induced p53 inhibits IEC proliferation by upregulating NDRG1 expression following polyamine depletion. Polyamines 126-135 tumor protein p53 Homo sapiens 52-55 17442733-5 2007 Depletion of cellular polyamines by inhibiting ornithine decarboxylase (ODC) with alpha-difluoromethylornithine not only induced p53 but also increased NDRG1 transcription as indicated by induction of the NDRG1 promoter activity and increased levels of NDRG1 mRNA and protein, all of which were prevented by using specific p53 siRNA and in cells with a targeted deletion of p53. Polyamines 22-32 tumor protein p53 Homo sapiens 129-132 17442733-5 2007 Depletion of cellular polyamines by inhibiting ornithine decarboxylase (ODC) with alpha-difluoromethylornithine not only induced p53 but also increased NDRG1 transcription as indicated by induction of the NDRG1 promoter activity and increased levels of NDRG1 mRNA and protein, all of which were prevented by using specific p53 siRNA and in cells with a targeted deletion of p53. Polyamines 22-32 tumor protein p53 Homo sapiens 323-326 17442733-5 2007 Depletion of cellular polyamines by inhibiting ornithine decarboxylase (ODC) with alpha-difluoromethylornithine not only induced p53 but also increased NDRG1 transcription as indicated by induction of the NDRG1 promoter activity and increased levels of NDRG1 mRNA and protein, all of which were prevented by using specific p53 siRNA and in cells with a targeted deletion of p53. Polyamines 22-32 tumor protein p53 Homo sapiens 323-326 17442733-6 2007 In contrast, increased levels of cellular polyamines by ectopic expression of the ODC gene decreased p53 and repressed expression of NDRG1. Polyamines 42-52 tumor protein p53 Homo sapiens 101-104 17442733-7 2007 Consistently, polyamine depletion-induced activation of the NDRG1-promoter was decreased when p53-binding sites within the NDRG1 proximal promoter region were deleted. Polyamines 14-23 tumor protein p53 Homo sapiens 94-97 16690610-0 2006 Polyamine depletion increases cytoplasmic levels of RNA-binding protein HuR leading to stabilization of nucleophosmin and p53 mRNAs. Polyamines 0-9 tumor protein p53 Homo sapiens 122-125 16690610-1 2006 Polyamines are essential for maintaining normal intestinal epithelial integrity, an effect that relies, at least in part, on their ability to keep low levels of nucleophosmin (NPM) and p53 mRNAs. Polyamines 0-10 tumor protein p53 Homo sapiens 185-188 16690610-6 2006 HuR silencing rendered the NPM and p53 mRNAs unstable and prevented increases in NPM and p53 mRNA and protein in polyamine-deficient cells. Polyamines 113-122 tumor protein p53 Homo sapiens 89-92 16690610-7 2006 These results indicate that polyamines modulate cytoplasmic HuR levels in intestinal epithelial cells, in turn controlling the stability of the NPM and p53 mRNAs and influencing NPM and p53 protein levels. Polyamines 28-38 tumor protein p53 Homo sapiens 152-155 16690610-7 2006 These results indicate that polyamines modulate cytoplasmic HuR levels in intestinal epithelial cells, in turn controlling the stability of the NPM and p53 mRNAs and influencing NPM and p53 protein levels. Polyamines 28-38 tumor protein p53 Homo sapiens 186-189 15180186-0 2004 Polyamine biosynthesis in relation to K-ras and p-53 mutations in colorectal carcinoma. Polyamines 0-9 tumor protein p53 Homo sapiens 48-52 15180186-10 2004 Polyamine biosynthesis was significantly higher in cancers showing K-ras mutation, either with or without p53 mutation [K-ras(+)/p53(-) and K-ras(+)/p53(+)], compared to samples with K-ras wild type [K-ras(-)/p53(-) and K-ras(-)/p53(+)]. Polyamines 0-9 tumor protein p53 Homo sapiens 106-109 15180186-10 2004 Polyamine biosynthesis was significantly higher in cancers showing K-ras mutation, either with or without p53 mutation [K-ras(+)/p53(-) and K-ras(+)/p53(+)], compared to samples with K-ras wild type [K-ras(-)/p53(-) and K-ras(-)/p53(+)]. Polyamines 0-9 tumor protein p53 Homo sapiens 129-132 15180186-10 2004 Polyamine biosynthesis was significantly higher in cancers showing K-ras mutation, either with or without p53 mutation [K-ras(+)/p53(-) and K-ras(+)/p53(+)], compared to samples with K-ras wild type [K-ras(-)/p53(-) and K-ras(-)/p53(+)]. Polyamines 0-9 tumor protein p53 Homo sapiens 129-132 15180186-10 2004 Polyamine biosynthesis was significantly higher in cancers showing K-ras mutation, either with or without p53 mutation [K-ras(+)/p53(-) and K-ras(+)/p53(+)], compared to samples with K-ras wild type [K-ras(-)/p53(-) and K-ras(-)/p53(+)]. Polyamines 0-9 tumor protein p53 Homo sapiens 129-132 15180186-12 2004 CONCLUSIONS: The present study provides evidence of a close relationship between K-ras mutation and polyamine biosynthesis in human colorectal carcinoma in a way that is largely p53 independent. Polyamines 100-109 tumor protein p53 Homo sapiens 178-181 8626797-6 1996 Furthermore, we found that amino acids 100-150 of p53 can function as an independent domain to induce Trypanosoma brucei ODC, a stable protein, to be degraded in vivo or, by cooperating with an antizyme binding domain of ODC, to confer polyamine-dependent regulation. Polyamines 236-245 tumor protein p53 Homo sapiens 50-53 10047792-0 1998 Polyamine analogue-mediated cell cycle responses in human melanoma cells involves the p53, p21, Rb regulatory pathway. Polyamines 0-9 tumor protein p53 Homo sapiens 86-89 10713709-8 2000 These data indicate that WR1065, a polyamine analog with thiol anti-oxidant properties, activates a cell cycle check-point involving p53. Polyamines 35-44 tumor protein p53 Homo sapiens 133-136 10096560-0 1999 Polyamine analogue induction of the p53-p21WAF1/CIP1-Rb pathway and G1 arrest in human melanoma cells. Polyamines 0-9 tumor protein p53 Homo sapiens 36-39 10096560-9 1999 Rather, these cells rapidly underwent programmed cell death within 48 h. Overall, these findings provide the first indication of the cell cycle regulatory pathways by which polyamine antagonists such as analogues might inhibit growth in cells containing wild-type p53 and further suggest a mechanistic basis for differential cellular responses to these agents. Polyamines 173-182 tumor protein p53 Homo sapiens 264-267 27698118-0 2016 Activation of SAT1 engages polyamine metabolism with p53-mediated ferroptotic responses. Polyamines 27-36 tumor protein p53 Homo sapiens 53-56 31086338-0 2019 Publisher Correction: p53 regulation of ammonia metabolism through urea cycle controls polyamine biosynthesis. Polyamines 87-96 tumor protein p53 Homo sapiens 22-25 30842655-0 2019 p53 regulation of ammonia metabolism through urea cycle controls polyamine biosynthesis. Polyamines 65-74 tumor protein p53 Homo sapiens 0-3 29316508-0 2018 Synthesis and biological evaluation of naphthalimide-polyamine conjugates modified by alkylation as anticancer agents through p53 pathway. Polyamines 53-62 tumor protein p53 Homo sapiens 126-129 27698118-8 2016 Thus, our findings uncover a metabolic target of p53 involved in ferroptotic cell death and provide insight into the regulation of polyamine metabolism and ferroptosis-mediated tumor suppression. Polyamines 131-140 tumor protein p53 Homo sapiens 49-52 26835380-8 2015 Moreover, polyamine depletion regimens exert potent anti-tumor activity in pre-clinical models of established neuroblastoma as well, in combination with numerous chemotherapeutic agents and even in tumors with unfavorable genetic features such as MYCN, ALK or TP53 mutation. Polyamines 10-19 tumor protein p53 Homo sapiens 260-264 25311224-7 2015 The resistant profile caused by p53 defect also caused a cell type-specific response to PA pool depletion and SSAT overexpression. Polyamines 88-90 tumor protein p53 Homo sapiens 32-35