PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33508133-0 2021 Broad-spectrum rescue compounds for structural p53 mutations: perspective on "Arsenic trioxide rescues structural p53 mutations through a cryptic allosteric site". Arsenic Trioxide 78-94 tumor protein p53 Homo sapiens 47-50 33508133-0 2021 Broad-spectrum rescue compounds for structural p53 mutations: perspective on "Arsenic trioxide rescues structural p53 mutations through a cryptic allosteric site". Arsenic Trioxide 78-94 tumor protein p53 Homo sapiens 114-117 33561393-3 2021 discover a new role for an old drug, arsenic trioxide, in binding and stabilizing p53. Arsenic Trioxide 37-53 tumor protein p53 Homo sapiens 82-85 29910624-11 2018 Conclusion: The present results show that AZT could increase the sensitization of As2O3 for inhibiting proliferation and promoting apoptosis of HepG2 cells through regulating the expression of Egr-1, which may control the expression of p53 and caspase-3. Arsenic Trioxide 82-87 tumor protein p53 Homo sapiens 236-239 32017938-0 2020 Long non-coding RNA ROR confers arsenic trioxide resistance to HepG2 cells by inhibiting p53 expression. Arsenic Trioxide 32-48 tumor protein p53 Homo sapiens 89-92 32017938-4 2020 In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells. Arsenic Trioxide 65-81 tumor protein p53 Homo sapiens 219-222 32017938-4 2020 In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells. Arsenic Trioxide 148-164 tumor protein p53 Homo sapiens 111-114 32017938-4 2020 In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells. Arsenic Trioxide 148-164 tumor protein p53 Homo sapiens 219-222 32017938-4 2020 In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells. Arsenic Trioxide 148-164 tumor protein p53 Homo sapiens 111-114 32017938-4 2020 In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells. Arsenic Trioxide 148-164 tumor protein p53 Homo sapiens 219-222 32017938-7 2020 Through the knock-down of long non-coding RNA ROR by siRNA, we revealed that the activated long non-coding RNA ROR ameliorated arsenic trioxide-induced apoptosis by inhibiting P53 expression. Arsenic Trioxide 127-143 tumor protein p53 Homo sapiens 176-179 32017938-8 2020 Together, our study reported that long non-coding RNA ROR conferred arsenic trioxide resistance to liver cancer cells through inhibiting P53 expression, and long non-coding RNA ROR might be a novel sensitizing target for liver cancer treatment. Arsenic Trioxide 68-84 tumor protein p53 Homo sapiens 137-140 33357454-0 2021 Arsenic Trioxide Rescues Structural p53 Mutations through a Cryptic Allosteric Site. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 36-39 33357454-3 2021 Here we report the identification of small molecules, including arsenic trioxide (ATO), an established agent in treating acute promyelocytic leukemia, as cysteine-reactive compounds that rescue structural p53 mutations. Arsenic Trioxide 64-80 tumor protein p53 Homo sapiens 205-208 33357454-3 2021 Here we report the identification of small molecules, including arsenic trioxide (ATO), an established agent in treating acute promyelocytic leukemia, as cysteine-reactive compounds that rescue structural p53 mutations. Arsenic Trioxide 82-85 tumor protein p53 Homo sapiens 205-208 27638049-8 2016 Additionally, ATO treatment leads to p53-regulated mitochondrial apoptosis, where p53 phosphorylation plays a key role. Arsenic Trioxide 14-17 tumor protein p53 Homo sapiens 37-40 29535630-7 2018 HCT-116 colon carcinoma p53-/- knockout cells were 7.16-fold resistant toward As2O3 compared to wild-type cells. Arsenic Trioxide 78-83 tumor protein p53 Homo sapiens 24-27 29164574-12 2017 CONCLUSIONS: As2O3 can inhibit proliferation of glioma cells and induce its apoptosis, which may be correlated with down-regulation of expressions of apoptosis-related factors, Fas, FasL and Bax, and apoptosis-related proteins, p53, caspase-3 and caspase-9. Arsenic Trioxide 13-18 tumor protein p53 Homo sapiens 228-231 27638049-8 2016 Additionally, ATO treatment leads to p53-regulated mitochondrial apoptosis, where p53 phosphorylation plays a key role. Arsenic Trioxide 14-17 tumor protein p53 Homo sapiens 82-85 26579413-0 2014 ETME, a novel beta-elemene derivative, synergizes with arsenic trioxide in inducing apoptosis and cell cycle arrest in hepatocarcinoma cells via a p53-dependent pathway. Arsenic Trioxide 55-71 tumor protein p53 Homo sapiens 147-150 26440706-3 2016 Study objectives were to: 1) define the lowest safe dose of arsenic trioxide that transiently blocks p53 activation in patients and 2) assess the potential of LDA to decrease hematological toxicity from chemotherapy. Arsenic Trioxide 60-76 tumor protein p53 Homo sapiens 101-104 25444910-6 2015 By contrast, arsenic trioxide, which by inhibiting wild-type p53-induced phosphatase-1 that serves responses downstream of p53, and by depolymerizing tubulin, synergistically enhanced cisplatin cytotoxicity including loss of SP cells. Arsenic Trioxide 13-29 tumor protein p53 Homo sapiens 61-64 25116336-0 2014 Arsenic trioxide reactivates proteasome-dependent degradation of mutant p53 protein in cancer cells in part via enhanced expression of Pirh2 E3 ligase. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 72-75 25116336-4 2014 Previously, we found that arsenic trioxide (ATO), a drug for acute promyelocytic leukemia, degrades mutant p53 protein through a proteasome pathway. Arsenic Trioxide 26-42 tumor protein p53 Homo sapiens 107-110 25116336-4 2014 Previously, we found that arsenic trioxide (ATO), a drug for acute promyelocytic leukemia, degrades mutant p53 protein through a proteasome pathway. Arsenic Trioxide 44-47 tumor protein p53 Homo sapiens 107-110 25116336-8 2014 We also found that knockdown of Pirh2 inhibits, whereas ectopic expression of Pirh2 enhances, ATO-induced degradation of mutant p53 protein. Arsenic Trioxide 94-97 tumor protein p53 Homo sapiens 128-131 25116336-10 2014 Interestingly, we found that ATO cooperates with HSP90 or HDAC inhibitor to promote mutant p53 degradation and growth suppression in tumor cells. Arsenic Trioxide 29-32 tumor protein p53 Homo sapiens 91-94 25116336-11 2014 Together, these data suggest that ATO promotes mutant p53 degradation in part via induction of the Pirh2-dependent proteasome pathway. Arsenic Trioxide 34-37 tumor protein p53 Homo sapiens 54-57 24927258-0 2014 Increased growth-inhibitory and cytotoxic activity of arsenic trioxide in head and neck carcinoma cells with functional p53 deficiency and resistance to EGFR blockade. Arsenic Trioxide 54-70 tumor protein p53 Homo sapiens 120-123 24927258-4 2014 The causal relationship between p53 deficiency and ATO sensitivity was evaluated by reconstitution of wildtype p53 in p53-deficient SCCHN cells. Arsenic Trioxide 51-54 tumor protein p53 Homo sapiens 32-35 24927258-4 2014 The causal relationship between p53 deficiency and ATO sensitivity was evaluated by reconstitution of wildtype p53 in p53-deficient SCCHN cells. Arsenic Trioxide 51-54 tumor protein p53 Homo sapiens 111-114 24927258-4 2014 The causal relationship between p53 deficiency and ATO sensitivity was evaluated by reconstitution of wildtype p53 in p53-deficient SCCHN cells. Arsenic Trioxide 51-54 tumor protein p53 Homo sapiens 111-114 24927258-6 2014 RESULTS: Functional rather than structural defects in the p53 gene predisposed tumor cells to increased sensitivity to ATO. Arsenic Trioxide 119-122 tumor protein p53 Homo sapiens 58-61 24927258-7 2014 Reconstitution of wt p53 in p53-deficient SCCHN cells rendered them less sensitive to ATO treatment. Arsenic Trioxide 86-89 tumor protein p53 Homo sapiens 21-24 24927258-7 2014 Reconstitution of wt p53 in p53-deficient SCCHN cells rendered them less sensitive to ATO treatment. Arsenic Trioxide 86-89 tumor protein p53 Homo sapiens 28-31 24927258-9 2014 The inhibitory effect of ATO in p53-deficient tumor cells was mainly associated with DNA damage, G2/M arrest, upregulation of TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) receptors and apoptosis. Arsenic Trioxide 25-28 tumor protein p53 Homo sapiens 32-35 24927258-11 2014 CONCLUSIONS: Addition of ATO to treatment regimens for p53-deficient SCCHN and tumor recurrence after cetuximab-containing regimens might represent an attractive strategy in SCCHN. Arsenic Trioxide 25-28 tumor protein p53 Homo sapiens 55-58 25485499-6 2014 Furthermore, for the first time we demonstrated that Arsenic trioxide, which was previously shown to suppress mutant p53 protein level, exhibits proteasome inhibitory activity. Arsenic Trioxide 53-69 tumor protein p53 Homo sapiens 117-120 24833880-1 2014 AIM: To investigate the changes in apoptosis in gastrointestinal cancer cells from patients with gastrointestinal cancers treated with arsenic trioxide (As2O3); and to study the possible molecular mechanisms of such changes by detecting the expression levels of p53 and Bcl-2. Arsenic Trioxide 135-151 tumor protein p53 Homo sapiens 262-265 23255470-3 2014 In the NuLi-1 immortalized human lung epithelial cell line with p53 and pRb deficiency, exposure to low doses of arsenic trioxide for 72 h promoted cell proliferation and upregulated the gene transcription levels of FOXM1, CDC6, CDC25A, and cyclin D1, which are both critical cell cycle regulatory genes and proto-oncogenes. Arsenic Trioxide 113-129 tumor protein p53 Homo sapiens 64-67 23255470-9 2014 These results showed for the first time that chronic exposure to low doses of arsenic trioxide promoted lung carcinogenicity, in part by aberrantly upregulating FOXM1 and its associated oncogenes, when the tumor suppressor genes p53 and pRb were inactivated. Arsenic Trioxide 78-94 tumor protein p53 Homo sapiens 229-232 24884809-3 2014 METHODS: Mutation detection of p53 gene in arsenic trioxide resistant HCC cell lines was performed. Arsenic Trioxide 43-59 tumor protein p53 Homo sapiens 31-34 24884809-6 2014 RESULTS: The acquisition of p53 mutation contributed to arsenic trioxide resistance and enhanced metastatic potential of HCC cells. Arsenic Trioxide 56-72 tumor protein p53 Homo sapiens 28-31 24884809-7 2014 Mutant p53 (Mutp53) silence could re-sensitize HCC resistant cells to arsenic trioxide and inhibit the metastatic activities, while mutp53 overexpression showed the opposite effects. Arsenic Trioxide 70-86 tumor protein p53 Homo sapiens 7-10 24884809-11 2014 CONCLUSIONS: Acquisitions of p53 mutations contributed to the resistance of HCC to arsenic trioxide. Arsenic Trioxide 83-99 tumor protein p53 Homo sapiens 29-32 24399651-0 2014 The impact of arsenic trioxide and all-trans retinoic acid on p53 R273H-codon mutant glioblastoma. Arsenic Trioxide 14-30 tumor protein p53 Homo sapiens 62-65 24399651-6 2014 The results showed that U87-p53(R273H) cells generated more rapid neurosphere growth than U87-p53(wt) but inhibition of neurosphere proliferation was seen with both ATO and ATRA. Arsenic Trioxide 165-168 tumor protein p53 Homo sapiens 28-31 24399651-7 2014 U87-p53(R273H) neurospheres showed resistance to differentiation into glial cells and neuronal cells with ATO and ATRA exposure. Arsenic Trioxide 106-109 tumor protein p53 Homo sapiens 4-7 24399651-8 2014 ATO was able to generate apoptosis at high doses and proliferation of U87-p53(wt) and U87-p53(R273H) cells was reduced with ATO and ATRA in a dose-dependent manner. Arsenic Trioxide 0-3 tumor protein p53 Homo sapiens 74-77 24399651-8 2014 ATO was able to generate apoptosis at high doses and proliferation of U87-p53(wt) and U87-p53(R273H) cells was reduced with ATO and ATRA in a dose-dependent manner. Arsenic Trioxide 0-3 tumor protein p53 Homo sapiens 90-93 24399651-8 2014 ATO was able to generate apoptosis at high doses and proliferation of U87-p53(wt) and U87-p53(R273H) cells was reduced with ATO and ATRA in a dose-dependent manner. Arsenic Trioxide 124-127 tumor protein p53 Homo sapiens 74-77 24399651-8 2014 ATO was able to generate apoptosis at high doses and proliferation of U87-p53(wt) and U87-p53(R273H) cells was reduced with ATO and ATRA in a dose-dependent manner. Arsenic Trioxide 124-127 tumor protein p53 Homo sapiens 90-93 24399651-9 2014 Elevated pERK1/2 and p53 expression was seen in U87-p53(R273H) neurospheres, which could be reduced with ATO and ATRA treatment. Arsenic Trioxide 105-108 tumor protein p53 Homo sapiens 21-24 24399651-9 2014 Elevated pERK1/2 and p53 expression was seen in U87-p53(R273H) neurospheres, which could be reduced with ATO and ATRA treatment. Arsenic Trioxide 105-108 tumor protein p53 Homo sapiens 52-55 24738333-12 2014 Moreover, transcription and protein expression of bcl-2, NFKB, survivin, bax, p53 and caspase-3 of Raji cells were regulated at the most remarkable extent in ADM-As2O3, MNPs group as compared with other groups. Arsenic Trioxide 162-167 tumor protein p53 Homo sapiens 78-81 20953137-4 2010 In this study, the molecular mechanisms of ATO-induced myeloma apoptosis were explored on four myeloma cell lines of wild type or mutant p53 status and also on six primary myeloma cells. Arsenic Trioxide 43-46 tumor protein p53 Homo sapiens 137-140 24004656-3 2013 We used three human neuroblastoma cell lines (SH-SY5Y, IGR-N-91, LAN-1) that differ from their MYCN and p53 status to explore the intracellular events activated by As2O3 and involved in neurite outgrowth, a morphological marker of differentiation. Arsenic Trioxide 164-169 tumor protein p53 Homo sapiens 104-107 23337567-8 2013 Additionally, these effects of ATO on gamma-H2AX, Chk1, Chk2, p53, and p21(waf1/cip1) were reduced by an ATM inhibitor. Arsenic Trioxide 31-34 tumor protein p53 Homo sapiens 62-65 21792014-7 2011 The contribution of YY1 to As2O3-induced p53 activation and apoptosis was also examined by Western blot and cell cycle analysis. Arsenic Trioxide 27-32 tumor protein p53 Homo sapiens 41-44 24211095-0 2013 Arsenic trioxide induces apoptosis in B-cell chronic lymphocytic leukemic cells through down-regulation of survivin via the p53-dependent signaling pathway. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 124-127 24211095-4 2013 WSU-CLL cells treated with 2muM As2O3 showed survivin down-regulation and p53 up-regulation. Arsenic Trioxide 32-37 tumor protein p53 Homo sapiens 74-77 24211095-6 2013 p53 inhibition by siRNA prevented the down-regulation of survivin by As2O3 and prevented the As2O3-induced cytotoxicity of WSU-CLL cells. Arsenic Trioxide 69-74 tumor protein p53 Homo sapiens 0-3 24211095-6 2013 p53 inhibition by siRNA prevented the down-regulation of survivin by As2O3 and prevented the As2O3-induced cytotoxicity of WSU-CLL cells. Arsenic Trioxide 93-98 tumor protein p53 Homo sapiens 0-3 21308489-0 2012 Arsenic trioxide induces apoptosis of p53 null osteosarcoma MG63 cells through the inhibition of catalase. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 38-41 21308489-1 2012 This study is aimed at investigating the effect of arsenic trioxide (ATO) on p53 null human osteosarcoma MG63 cells and the mechanisms underlying the effect. Arsenic Trioxide 51-67 tumor protein p53 Homo sapiens 77-80 21308489-1 2012 This study is aimed at investigating the effect of arsenic trioxide (ATO) on p53 null human osteosarcoma MG63 cells and the mechanisms underlying the effect. Arsenic Trioxide 69-72 tumor protein p53 Homo sapiens 77-80 21454520-5 2011 In this study, we found that wild type p53 is induced by arsenic trioxide in tumor cells, consistent with published studies. Arsenic Trioxide 57-73 tumor protein p53 Homo sapiens 39-42 21454520-7 2011 We also found that arsenic trioxide decreases the stability of mutant p53 protein through a proteasomal pathway, and blockage of mutant p53 nuclear export can alleviate the arsenic-induced mutant p53 degradation. Arsenic Trioxide 19-35 tumor protein p53 Homo sapiens 70-73 20953137-7 2010 ATO treatment increased mRNA levels of interferon regulatory factor-1 and TRAIL, as well as protein levels of caspase 8 and cleaved caspase 3, indicating the involvement of the extrinsic apoptotic pathway in the mutated p53 myeloma cells. Arsenic Trioxide 0-3 tumor protein p53 Homo sapiens 220-223 20953137-8 2010 ATO also activated caspases 3 and 9, indicating involvement of the intrinsic apoptotic pathway in the wild type p53 myeloma cells. Arsenic Trioxide 0-3 tumor protein p53 Homo sapiens 112-115 20953137-10 2010 Together, our data suggest that ATO induces apoptosis in MM through either extrinsic or intrinsic signaling pathway, depending on the p53 genetic background. Arsenic Trioxide 32-35 tumor protein p53 Homo sapiens 134-137 17530438-0 2008 Arsenic trioxide induces different gene expression profiles of genes related to growth and apoptosis in glioma cells dependent on the p53 status. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 134-137 19444595-0 2009 Modulation of p53, c-fos, RARE, cyclin A, and cyclin D1 expression in human leukemia (HL-60) cells exposed to arsenic trioxide. Arsenic Trioxide 110-126 tumor protein p53 Homo sapiens 14-17 19587434-6 2009 Effect of arsenic trioxide and adriamycin on the mutant p53 expression in Raji cells was detected by semi-quantitive RT-PCR. Arsenic Trioxide 10-26 tumor protein p53 Homo sapiens 56-59 20377131-4 2010 Flow cytometry analyses demonstrated an increase in apoptosis following combined treatment with As2O3 and Ad-PML for 24 h, which was correlated with increased p53 and decreased Bcl-2 expression. Arsenic Trioxide 96-101 tumor protein p53 Homo sapiens 159-162 19457607-0 2009 Arsenic trioxide induces apoptosis and G2/M phase arrest by inducing Cbl to inhibit PI3K/Akt signaling and thereby regulate p53 activation. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 124-127 19457607-4 2009 ATO-induced G2/M phase arrest and p53 degradation in gastric cancer MGC803 cells. Arsenic Trioxide 0-3 tumor protein p53 Homo sapiens 34-37 18668508-8 2008 The marked correlation between ATO-induced mitotic arrest and apoptosis indicates that the induction of apoptosis by ATO was highly dependent on the functional activation of the spindle checkpoint in cancer cells lacking normal p53 function. Arsenic Trioxide 31-34 tumor protein p53 Homo sapiens 228-231 18668508-8 2008 The marked correlation between ATO-induced mitotic arrest and apoptosis indicates that the induction of apoptosis by ATO was highly dependent on the functional activation of the spindle checkpoint in cancer cells lacking normal p53 function. Arsenic Trioxide 117-120 tumor protein p53 Homo sapiens 228-231 18583568-2 2008 In HMCLs retaining a functional p53, PD treatment greatly enhances the ATO-induced p53 accumulation and p73, a p53 paralog, cooperates with p53 in caspase activation and apoptosis induction. Arsenic Trioxide 71-74 tumor protein p53 Homo sapiens 83-86 18583568-2 2008 In HMCLs retaining a functional p53, PD treatment greatly enhances the ATO-induced p53 accumulation and p73, a p53 paralog, cooperates with p53 in caspase activation and apoptosis induction. Arsenic Trioxide 71-74 tumor protein p53 Homo sapiens 83-86 18583568-2 2008 In HMCLs retaining a functional p53, PD treatment greatly enhances the ATO-induced p53 accumulation and p73, a p53 paralog, cooperates with p53 in caspase activation and apoptosis induction. Arsenic Trioxide 71-74 tumor protein p53 Homo sapiens 83-86 18482988-2 2008 It has been reported that arsenic trioxide (ATO), a potent cancer chemotherapeutic agent, in particular for acute promyelocytic leukemia, activates the Chk2/p53 pathway, leading to apoptosis. Arsenic Trioxide 44-47 tumor protein p53 Homo sapiens 157-160 18482988-3 2008 ATO is also known to activate the p38 MAPK/p53 pathway. Arsenic Trioxide 0-3 tumor protein p53 Homo sapiens 43-46 18482988-0 2008 Arsenic trioxide augments Chk2/p53-mediated apoptosis by inhibiting oncogenic Wip1 phosphatase. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 31-34 18482988-7 2008 Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo. Arsenic Trioxide 18-21 tumor protein p53 Homo sapiens 49-52 18482988-2 2008 It has been reported that arsenic trioxide (ATO), a potent cancer chemotherapeutic agent, in particular for acute promyelocytic leukemia, activates the Chk2/p53 pathway, leading to apoptosis. Arsenic Trioxide 26-42 tumor protein p53 Homo sapiens 157-160 18482988-7 2008 Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo. Arsenic Trioxide 18-21 tumor protein p53 Homo sapiens 66-69 18482988-7 2008 Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo. Arsenic Trioxide 179-182 tumor protein p53 Homo sapiens 49-52 18482988-7 2008 Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo. Arsenic Trioxide 179-182 tumor protein p53 Homo sapiens 66-69 17332940-0 2007 Arsenic trioxide induces p53-dependent apoptotic signals in myeloma cells with SiRNA-silenced p53: MAP kinase pathway is preferentially activated in cells expressing inactivated p53. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 25-28 18167198-0 2007 Effects of HBV X gene and arsenic trioxide on the expression of p53 in cultured HepG2 cells. Arsenic Trioxide 26-42 tumor protein p53 Homo sapiens 64-67 18167198-2 2007 In recent years, effects of arsenic trioxide (As2O3) on the expression of p53 protein have been widely studied, while little is known about the activity of p53 protein. Arsenic Trioxide 28-44 tumor protein p53 Homo sapiens 74-77 18167198-2 2007 In recent years, effects of arsenic trioxide (As2O3) on the expression of p53 protein have been widely studied, while little is known about the activity of p53 protein. Arsenic Trioxide 46-51 tumor protein p53 Homo sapiens 74-77 18167198-3 2007 This study was undertaken to delineate the effect of HBV X gene and As2O3 on p53 protein expression (level and activity) in HepG2 cells by small hairpin RNA (shRNA)-mediated RNA interference (RNAi) technique. Arsenic Trioxide 68-73 tumor protein p53 Homo sapiens 77-80 18167198-9 2007 The effect of As2O3 on p53 protein expression and activity was re-observed. Arsenic Trioxide 14-19 tumor protein p53 Homo sapiens 23-26 18167198-10 2007 RESULTS: Total p53 protein level was up-regulated and its relative activity ratio was enhanced by As2O3 in HepG2 and HepG2-X cells. Arsenic Trioxide 98-103 tumor protein p53 Homo sapiens 15-18 18167198-11 2007 The total p53 protein level induced by As2O3 was up-regulated by HBV X gene expression, while its relative activity was significantly suppressed. Arsenic Trioxide 39-44 tumor protein p53 Homo sapiens 10-13 18167198-13 2007 CONCLUSIONS: As2O3 up-regulates p53 protein expression and enhance its activity. Arsenic Trioxide 13-18 tumor protein p53 Homo sapiens 32-35 18167198-14 2007 HBV X up-regulates As2O3 induced-p53 protein expression while suppresses its activity. Arsenic Trioxide 19-24 tumor protein p53 Homo sapiens 33-36 17332940-0 2007 Arsenic trioxide induces p53-dependent apoptotic signals in myeloma cells with SiRNA-silenced p53: MAP kinase pathway is preferentially activated in cells expressing inactivated p53. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 94-97 17332940-0 2007 Arsenic trioxide induces p53-dependent apoptotic signals in myeloma cells with SiRNA-silenced p53: MAP kinase pathway is preferentially activated in cells expressing inactivated p53. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 94-97 16950207-6 2006 Combined sulindac/ATO treatment also activated p53 expression, and inhibition of p53 expression by small interfering RNA (siRNA) prevented sulindac/ATO-induced down-regulation of survivin, suggesting that survivin expression is negatively regulated by p53. Arsenic Trioxide 18-21 tumor protein p53 Homo sapiens 47-50 17487067-12 2007 HepG2 cells exposed to arsenic trioxide and PFT-alpha showed expression of only the P53 and PCNA genes. Arsenic Trioxide 23-39 tumor protein p53 Homo sapiens 84-87 16950207-6 2006 Combined sulindac/ATO treatment also activated p53 expression, and inhibition of p53 expression by small interfering RNA (siRNA) prevented sulindac/ATO-induced down-regulation of survivin, suggesting that survivin expression is negatively regulated by p53. Arsenic Trioxide 148-151 tumor protein p53 Homo sapiens 81-84 16950207-6 2006 Combined sulindac/ATO treatment also activated p53 expression, and inhibition of p53 expression by small interfering RNA (siRNA) prevented sulindac/ATO-induced down-regulation of survivin, suggesting that survivin expression is negatively regulated by p53. Arsenic Trioxide 148-151 tumor protein p53 Homo sapiens 81-84 17064470-0 2006 [Study of effects of HBV X gene and As2O3 on expression and activity of p53 in HepG2 cells with shRNA]. Arsenic Trioxide 36-41 tumor protein p53 Homo sapiens 72-75 16646077-0 2006 Clinically tolerable concentrations of arsenic trioxide induce p53-independent cell death and repress NF-kappa B activation in Ewing sarcoma cells. Arsenic Trioxide 39-55 tumor protein p53 Homo sapiens 63-66 15904916-5 2005 Results also indicate that after arsenic trioxide treatment, p53 protein levels increased significantly and also could bind directly at the telomere t-loop junction. Arsenic Trioxide 33-49 tumor protein p53 Homo sapiens 61-64 16891316-9 2006 Based on this, we propose that a pathway composed of ATR, PML, Chk2, and p53 plays a role in ATO-mediated apoptosis, a notion that is consistent with the observation that Chk2 is genetically intact and mutations in the p53 gene are extremely rare in APL. Arsenic Trioxide 93-96 tumor protein p53 Homo sapiens 73-76 16891316-9 2006 Based on this, we propose that a pathway composed of ATR, PML, Chk2, and p53 plays a role in ATO-mediated apoptosis, a notion that is consistent with the observation that Chk2 is genetically intact and mutations in the p53 gene are extremely rare in APL. Arsenic Trioxide 93-96 tumor protein p53 Homo sapiens 219-222 16283431-0 2006 Opposite effect of ERK1/2 and JNK on p53-independent p21WAF1/CIP1 activation involved in the arsenic trioxide-induced human epidermoid carcinoma A431 cellular cytotoxicity. Arsenic Trioxide 93-109 tumor protein p53 Homo sapiens 37-40 16467208-6 2006 High doses of ATO induced p53 accumulation in 11 of 21 patients. Arsenic Trioxide 14-17 tumor protein p53 Homo sapiens 26-29 14726646-3 2004 We have previously shown that ATO is a potent inducer of apoptosis in myeloma cells expressing mutant p53 engaging both the intrinsic and extrinsic apoptotic pathways. Arsenic Trioxide 30-33 tumor protein p53 Homo sapiens 102-105 15225615-0 2004 A P53 target gene, PIG11, contributes to chemosensitivity of cells to arsenic trioxide. Arsenic Trioxide 70-86 tumor protein p53 Homo sapiens 2-5 15225615-3 2004 Recent data demonstrated that PIG11 was up-regulated markedly in arsenic trioxide induced apoptosis by DDRT-PCR, suggesting a new class of p53 target genes that sensitize cells to the effects of chemotherapeutic agents. Arsenic Trioxide 65-81 tumor protein p53 Homo sapiens 139-142 15007384-6 2004 The apoptosis induction due to As2O3 treatment of LNCaP cell correlated with the activation of JNK and p38 and induction of p53 protein. Arsenic Trioxide 31-36 tumor protein p53 Homo sapiens 124-127 15131059-1 2004 PURPOSE: On the basis of clinical studies showing that arsenic trioxide (As(2)O(3)), via an apoptotic mechanism, and with minimal toxicity induces complete remission in patients with refractory acute promyelocytic leukemia and that multidrug-resistant and p53-mutated neuroblastoma cells are sensitive to As(2)O(3) both in vitro and in vivo, we searched for molecular mechanisms involved in the As(2)O(3)-induced neuroblastoma cell death. Arsenic Trioxide 55-71 tumor protein p53 Homo sapiens 256-259 15131059-1 2004 PURPOSE: On the basis of clinical studies showing that arsenic trioxide (As(2)O(3)), via an apoptotic mechanism, and with minimal toxicity induces complete remission in patients with refractory acute promyelocytic leukemia and that multidrug-resistant and p53-mutated neuroblastoma cells are sensitive to As(2)O(3) both in vitro and in vivo, we searched for molecular mechanisms involved in the As(2)O(3)-induced neuroblastoma cell death. Arsenic Trioxide 73-82 tumor protein p53 Homo sapiens 256-259 12531793-0 2003 Arsenic trioxide-induced apoptosis in myeloma cells: p53-dependent G1 or G2/M cell cycle arrest, activation of caspase-8 or caspase-9, and synergy with APO2/TRAIL. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 53-56 14682389-12 2003 The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p<0.05) between treated and control cells. Arsenic Trioxide 33-49 tumor protein p53 Homo sapiens 4-7 12883691-3 2003 In this study, we found PIG11, a p53-induced gene, was upregulated markedly by As2O3 using the technique of differential display reverse transcriptase PCR (DDRT-PCR). Arsenic Trioxide 79-84 tumor protein p53 Homo sapiens 33-36 12915590-4 2003 Cellular stress and DNA damage caused by UV-radiation, downregulation of the proteasome and arsenic trioxide promoted Mdm2 and PML damage-specific nuclear relocalization and interaction in a p53-independent manner. Arsenic Trioxide 92-108 tumor protein p53 Homo sapiens 191-194 12851490-0 2003 Arsenic trioxide selectively induces early and extensive apoptosis via the APO2/caspase-8 pathway engaging the mitochondrial pathway in myeloma cells with mutant p53. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 162-165 12851490-2 2003 We have previously shown that ATO induces apoptosis in myeloma cells in two different modes depending on p53 status in the cells. Arsenic Trioxide 30-33 tumor protein p53 Homo sapiens 105-108 12851490-3 2003 In cells expressing mutated p53, ATO induced, G2/M arrest and activation caspase 8 and 3 and rapid and extensive apoptosis. Arsenic Trioxide 33-36 tumor protein p53 Homo sapiens 28-31 12531793-4 2003 We tested the effect of ATO on 7 myeloma cell lines with varying p53 status and report that in cells with mutated p53, ATO induced rapid and extensive (more than 90%) apoptosis in a time- and dose-dependent manner concomitant with arrest of cells in G(2)/M phase of the cell cycle. Arsenic Trioxide 119-122 tumor protein p53 Homo sapiens 65-68 12531793-4 2003 We tested the effect of ATO on 7 myeloma cell lines with varying p53 status and report that in cells with mutated p53, ATO induced rapid and extensive (more than 90%) apoptosis in a time- and dose-dependent manner concomitant with arrest of cells in G(2)/M phase of the cell cycle. Arsenic Trioxide 119-122 tumor protein p53 Homo sapiens 114-117 12531793-5 2003 Myeloma cells with wild-type (wt) p53 were relatively resistant to ATO with maximal apoptosis of about 40% concomitant with partial arrest of cells in G(1) and up-regulation of p21. Arsenic Trioxide 67-70 tumor protein p53 Homo sapiens 34-37 12531793-6 2003 The use of caspase blocking peptides, fluorescence-tagged caspase-specific substrate peptides, and Western immunoblotting confirmed the involvement of primarily caspase-8 and -3 in ATO-induced apoptosis in myeloma cells with mutated p53 and primarily caspase-9 and -3 in cells expressing wt p53. Arsenic Trioxide 181-184 tumor protein p53 Homo sapiens 233-236 12531793-6 2003 The use of caspase blocking peptides, fluorescence-tagged caspase-specific substrate peptides, and Western immunoblotting confirmed the involvement of primarily caspase-8 and -3 in ATO-induced apoptosis in myeloma cells with mutated p53 and primarily caspase-9 and -3 in cells expressing wt p53. Arsenic Trioxide 181-184 tumor protein p53 Homo sapiens 291-294 12490120-0 2002 [Arsenic trioxide induced apoptosis and expression of p53 and bcl-2 genes in human small cell lung cancer cells]. Arsenic Trioxide 1-17 tumor protein p53 Homo sapiens 54-57 12641444-7 2003 Of this group, arsenic trioxide was the strongest inducer of cellular p53, while dimethylarsinic acid, iododimethylarsine, and sodium arsenite also caused p53 induction in a dose- and time-dependent manner. Arsenic Trioxide 15-31 tumor protein p53 Homo sapiens 70-73 12641444-7 2003 Of this group, arsenic trioxide was the strongest inducer of cellular p53, while dimethylarsinic acid, iododimethylarsine, and sodium arsenite also caused p53 induction in a dose- and time-dependent manner. Arsenic Trioxide 15-31 tumor protein p53 Homo sapiens 155-158 11150309-0 2001 Opposite effect of NF-kappa B and c-Jun N-terminal kinase on p53-independent GADD45 induction by arsenite. Arsenic Trioxide 97-105 tumor protein p53 Homo sapiens 61-64 12430174-6 2002 Protein levels of p53 and cleavage of poly(ADP)-ribose polymerase were increased in a dose-dependent manner following treatment of As2O3. Arsenic Trioxide 131-136 tumor protein p53 Homo sapiens 18-21 12063549-8 2002 As2O3 induced an increase in p53 level and a decrease in level of cyclin B1 combined with cell arrest at G2/M in both cell lines. Arsenic Trioxide 0-5 tumor protein p53 Homo sapiens 29-32 11150309-2 2001 Using cells derived from human bronchial epithelial cells, we demonstrate that NF-kappaB and c-Jun N-terminal kinase (JNK) reciprocally regulate arsenic trioxide (arsenite)-induced, p53-independent expression of GADD45 protein, a cell cycle checkpoint protein that arrests cells at the G(2)/M phase transition. Arsenic Trioxide 145-161 tumor protein p53 Homo sapiens 182-185 11150309-2 2001 Using cells derived from human bronchial epithelial cells, we demonstrate that NF-kappaB and c-Jun N-terminal kinase (JNK) reciprocally regulate arsenic trioxide (arsenite)-induced, p53-independent expression of GADD45 protein, a cell cycle checkpoint protein that arrests cells at the G(2)/M phase transition. Arsenic Trioxide 163-171 tumor protein p53 Homo sapiens 182-185 35487055-9 2022 Generally, both cell lines treated with the combination of Curcumin and As2O3 displayed decreased angiogenesis genes (VEGFA and VEGFC), apoptosis genes (BAX and Bcl2), and prostate cancer marker (KLK2), the zinc-finger protein (SNAIL); and an increase in expression (P < 0.05) of cell-cell adhesion molecule (E-cadherin) and tumor suppressor gene (P53) genes. Arsenic Trioxide 72-77 tumor protein p53 Homo sapiens 348-351 34880920-15 2021 In the arsenic trioxide-target-pathway-HCC network, targets such as AKT1, RAF1, RELA, TP53, and PTEN had a higher degree. Arsenic Trioxide 7-23 tumor protein p53 Homo sapiens 86-90 11146441-0 2001 Arsenic trioxide induces apoptosis in human gastric cancer cells through up-regulation of p53 and activation of caspase-3. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 90-93 11798837-2 2000 METHODS: Human lung adenocarcinoma cell line GLC-82 was transfected with adenovirus-mediated p53 gene (Ad-p53) combining with administration of either kind of chemotherapeutic agents-cisplatin (CDDP) and arsenic trioxide (As(2)O(3)). Arsenic Trioxide 204-220 tumor protein p53 Homo sapiens 93-96 15622746-5 1997 Furthermore, As2O3 effectively down-regulated the expression of bcl-2 gene without changing the mRNA levels of other apoptosis-associated genes (including p53, c-myc, bax and bcl-XL). Arsenic Trioxide 13-18 tumor protein p53 Homo sapiens 155-158 34800879-6 2022 Generally, both cell lines treated with the combination of Flutamide and ATO showed a decrease in expression of KLK2, angiogenesis genes (VEGFA and VEGFC), and apoptosis gene (Bcl2), and an increase in expression of E-cadherin and P53 genes; however, contradictory findings were found regarding SNAIL expression in LNCaP and PC3 cells. Arsenic Trioxide 73-76 tumor protein p53 Homo sapiens 231-234 34255251-7 2021 Real-time RT-PCR indicated that the co-administration of Schiff base oxovanadium complex 40 microg/ml and arsenic trioxide 0.001 microM could increase the expression of P53 and P21 genes by 3.76 +- 0.19 and 6.57 +- 1.29 fold change, respectively to the control sample. Arsenic Trioxide 106-122 tumor protein p53 Homo sapiens 169-172 34476069-0 2021 Arsenic trioxide targets Hsp60, triggering degradation of p53 and survivin. Arsenic Trioxide 0-16 tumor protein p53 Homo sapiens 58-61 34476069-7 2021 Significantly, the binding of ATO to Hsp60 disrupts the formation of Hsp60-p53 and Hsp60-survivin complexes, resulting in degradation of p53 and survivin. Arsenic Trioxide 30-33 tumor protein p53 Homo sapiens 75-78 34476069-7 2021 Significantly, the binding of ATO to Hsp60 disrupts the formation of Hsp60-p53 and Hsp60-survivin complexes, resulting in degradation of p53 and survivin. Arsenic Trioxide 30-33 tumor protein p53 Homo sapiens 137-140