PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31871844-8 2019 Three drugs, mitomycin-C, doxorubicin and gemcitabine, were especially more sensitive to bladder cancer with the TP53 mutation. Mitomycin 13-24 tumor protein p53 Homo sapiens 113-117 24789349-8 2014 Notably, FANCF shRNA was able to increase p53 levels through activation of the JNK pathway in MMC-treated breast cancer cells. Mitomycin 94-97 tumor protein p53 Homo sapiens 42-45 30091208-8 2018 This implied that the deactivated Akt caused by MC/DMC was p53-dependent. Mitomycin 48-50 tumor protein p53 Homo sapiens 59-62 30091208-13 2018 In summary, MC/DMC regulate Akt activation in a p53-dependent manner. Mitomycin 12-14 tumor protein p53 Homo sapiens 48-51 27666201-0 2016 Mitomycin C and decarbamoyl mitomycin C induce p53-independent p21WAF1/CIP1 activation. Mitomycin 0-11 tumor protein p53 Homo sapiens 47-50 27666201-13 2016 Knocking down p53 in MCF-7 did not attenuate MC and DMC induced p21WAF1/CIP1 activation. Mitomycin 21-23 tumor protein p53 Homo sapiens 14-17 27323408-5 2016 LACE1 physically interacts with p53 and is necessary for mitomycin c-induced translocation of p53 into mitochondria. Mitomycin 57-68 tumor protein p53 Homo sapiens 32-35 27323408-5 2016 LACE1 physically interacts with p53 and is necessary for mitomycin c-induced translocation of p53 into mitochondria. Mitomycin 57-68 tumor protein p53 Homo sapiens 94-97 26354682-0 2015 Hypoxia Promotes Synergy between Mitomycin C and Bortezomib through a Coordinated Process of Bcl-xL Phosphorylation and Mitochondrial Translocation of p53. Mitomycin 33-44 tumor protein p53 Homo sapiens 151-154 30091208-2 2018 MC analog, 10-decarbamoyl mitomycin C (DMC), unlike MC, has stronger effects on cancer with p53 mutation. Mitomycin 0-2 tumor protein p53 Homo sapiens 92-95 30091208-2 2018 MC analog, 10-decarbamoyl mitomycin C (DMC), unlike MC, has stronger effects on cancer with p53 mutation. Mitomycin 40-42 tumor protein p53 Homo sapiens 92-95 30091208-3 2018 We previously demonstrated that MC/DMC could activate p21WAF 1/ CIP 1 in MCF-7 (p53-proficient) and K562 (p53-deficient) cells in a p53-independent mode. Mitomycin 32-34 tumor protein p53 Homo sapiens 80-83 30091208-3 2018 We previously demonstrated that MC/DMC could activate p21WAF 1/ CIP 1 in MCF-7 (p53-proficient) and K562 (p53-deficient) cells in a p53-independent mode. Mitomycin 32-34 tumor protein p53 Homo sapiens 106-109 30091208-3 2018 We previously demonstrated that MC/DMC could activate p21WAF 1/ CIP 1 in MCF-7 (p53-proficient) and K562 (p53-deficient) cells in a p53-independent mode. Mitomycin 32-34 tumor protein p53 Homo sapiens 106-109 28979810-5 2017 It was found that chemotherapy drugs, such as epirubicin (EPB) and mitomycin C (MMC), effectively blocked expression of PcG in p53-wild-type HepG2 cells but not in PLC/PRF5 and Hep3B cells with p53 mutation or deletion. Mitomycin 67-78 tumor protein p53 Homo sapiens 127-130 28979810-5 2017 It was found that chemotherapy drugs, such as epirubicin (EPB) and mitomycin C (MMC), effectively blocked expression of PcG in p53-wild-type HepG2 cells but not in PLC/PRF5 and Hep3B cells with p53 mutation or deletion. Mitomycin 67-78 tumor protein p53 Homo sapiens 194-197 28979810-5 2017 It was found that chemotherapy drugs, such as epirubicin (EPB) and mitomycin C (MMC), effectively blocked expression of PcG in p53-wild-type HepG2 cells but not in PLC/PRF5 and Hep3B cells with p53 mutation or deletion. Mitomycin 80-83 tumor protein p53 Homo sapiens 127-130 28979810-5 2017 It was found that chemotherapy drugs, such as epirubicin (EPB) and mitomycin C (MMC), effectively blocked expression of PcG in p53-wild-type HepG2 cells but not in PLC/PRF5 and Hep3B cells with p53 mutation or deletion. Mitomycin 80-83 tumor protein p53 Homo sapiens 194-197 26004085-10 2015 Our findings strongly indicate that concomitant inactivation of the p53- and pRB- pathways predict resistance towards anthracyclines and mitomycin in breast cancer in vivo. Mitomycin 137-146 tumor protein p53 Homo sapiens 68-71 25713207-8 2015 Finally, chromatin immunoprecipitation assays demonstrated p53 recruitment to the UGT2B7 p53 site upon exposure to mitomycin C, the most potent UGT2B7 inducer among the nine tested drugs. Mitomycin 115-126 tumor protein p53 Homo sapiens 59-62 25713207-8 2015 Finally, chromatin immunoprecipitation assays demonstrated p53 recruitment to the UGT2B7 p53 site upon exposure to mitomycin C, the most potent UGT2B7 inducer among the nine tested drugs. Mitomycin 115-126 tumor protein p53 Homo sapiens 89-92 24789349-9 2014 Furthermore, p53 inhibition using pifithrin-alpha abolished the induction of caspase-3 and PARP by FANCF shRNA and MMC, indicating that MMC-induced apoptosis is substantially enhanced by FANCF shRNA via p53-dependent mechanisms. Mitomycin 115-118 tumor protein p53 Homo sapiens 13-16 24789349-9 2014 Furthermore, p53 inhibition using pifithrin-alpha abolished the induction of caspase-3 and PARP by FANCF shRNA and MMC, indicating that MMC-induced apoptosis is substantially enhanced by FANCF shRNA via p53-dependent mechanisms. Mitomycin 115-118 tumor protein p53 Homo sapiens 203-206 22349266-4 2012 When treated with mitomycin C, p53-deficient cells, but not p53-expressing cells, showed a marked increase in ceramide levels. Mitomycin 18-29 tumor protein p53 Homo sapiens 31-34 24675086-0 2014 Chromosome breakage induced by the genotoxic agents mitomycin C and cytosine arabinoside is concentration and p53 dependent. Mitomycin 52-63 tumor protein p53 Homo sapiens 110-113 24675086-7 2014 Low levels of micronucleus and p53 induction were observed in TK6 cells treated with MMC. Mitomycin 85-88 tumor protein p53 Homo sapiens 31-34 22895172-0 2012 Mitomycin C potentiates TRAIL-induced apoptosis through p53-independent upregulation of death receptors: evidence for the role of c-Jun N-terminal kinase activation. Mitomycin 0-11 tumor protein p53 Homo sapiens 56-59 22895172-3 2012 We found that MMC not only potentiated TRAIL-induced apoptosis in HCT116 (p53-/-) colon cancer cells but also sensitized TRAIL-resistant colon cancer cells HT-29 to the cytokine both in vitro and in vivo. Mitomycin 14-17 tumor protein p53 Homo sapiens 74-77 23246812-0 2013 Functional characterisation of p53 mutants identified in breast cancers with suboptimal responses to anthracyclines or mitomycin. Mitomycin 119-128 tumor protein p53 Homo sapiens 31-34 23246812-2 2013 TP53 mutations, in particular those affecting the L2/L3 domains, are associated with resistance to anthracycline or mitomycin treatment in breast cancer patients. Mitomycin 116-125 tumor protein p53 Homo sapiens 0-4 22349266-7 2012 When inhibition of UGCG and treatment with mitomycin C were combined, p53-deficient, but not p53-expressing cells, showed a significant increase in cell death, suggesting that the regulation of sphingolipid metabolism could be used to sensitize cells to chemotherapeutic drugs. Mitomycin 43-54 tumor protein p53 Homo sapiens 70-73 20798760-5 2010 Specifically, 2,7-DAM is not cytotoxic and does not activate the p53 pathway while MC and DMC are cytotoxic and able to activate the p53 pathway. Mitomycin 83-85 tumor protein p53 Homo sapiens 133-136 22420423-0 2012 Low expression levels of ATM may substitute for CHEK2 /TP53 mutations predicting resistance towards anthracycline and mitomycin chemotherapy in breast cancer. Mitomycin 118-127 tumor protein p53 Homo sapiens 55-59 22420423-11 2012 CONCLUSIONS: Our data indicate loss of function of the ATM-Chk2-p53 cascade to be strongly associated with resistance to anthracycline/mitomycin-containing chemotherapy in breast cancer. Mitomycin 135-144 tumor protein p53 Homo sapiens 64-67 22076446-3 2012 For the first time, we report p53 up-regulation in 9/14 and Fas up-regulation in 7/9 TCCB patients during intravesical MMC treatment. Mitomycin 119-122 tumor protein p53 Homo sapiens 30-33 20798760-6 2010 DMC is more cytotoxic than MC and can also kill p53-deficient cells by inducing degradation of Checkpoint 1 protein, which is not seen with MC treatment of the p53-deficient cells. Mitomycin 1-3 tumor protein p53 Homo sapiens 48-51 20126473-3 2010 Our study showed that p53 mitochondrial translocation was found in mitomycin C (MMC)-treated HepG2. Mitomycin 67-78 tumor protein p53 Homo sapiens 22-25 20536192-1 2010 The mitomycin derivative 10-decarbamoyl mitomycin C (DMC) more rapidly activates a p53-independent cell death pathway than mitomycin C (MC). Mitomycin 4-13 tumor protein p53 Homo sapiens 83-86 20536192-1 2010 The mitomycin derivative 10-decarbamoyl mitomycin C (DMC) more rapidly activates a p53-independent cell death pathway than mitomycin C (MC). Mitomycin 40-51 tumor protein p53 Homo sapiens 83-86 20536192-1 2010 The mitomycin derivative 10-decarbamoyl mitomycin C (DMC) more rapidly activates a p53-independent cell death pathway than mitomycin C (MC). Mitomycin 54-56 tumor protein p53 Homo sapiens 83-86 20479887-5 2010 Camptothecin is a reported inhibitor of HIF-1alpha translation, while mitomycin C has been reported to induce p53-dependent HIF-1alpha degradation. Mitomycin 70-81 tumor protein p53 Homo sapiens 110-113 20479887-6 2010 In this study we demonstrate that the inhibitory effect of mitomycin C on HIF-1alpha protein expression is not dependent on p53 and protein degradation, but also involves HIF-1alpha translational regulation. Mitomycin 59-70 tumor protein p53 Homo sapiens 124-127 20126473-3 2010 Our study showed that p53 mitochondrial translocation was found in mitomycin C (MMC)-treated HepG2. Mitomycin 80-83 tumor protein p53 Homo sapiens 22-25 20126473-12 2010 In the low-dose MMC treatment, the increased mitochondrial p53, Bcl-xL, and Bcl-2 could attenuate apoptosis. Mitomycin 16-19 tumor protein p53 Homo sapiens 59-62 20126473-13 2010 However, in the high-dose MMC treatment, only the p53 translocated to the mitochondria and resulted in apoptosis progression. Mitomycin 26-29 tumor protein p53 Homo sapiens 50-53 18571879-6 2008 We also analyzed the splice patterns of apoptosis-related genes in p53-deficient U2OS cells following treatment with the genotoxic drug mitomycin C. Mitomycin 136-147 tumor protein p53 Homo sapiens 67-70 18697203-9 2008 Mitomycin treatment of MEF induced similar epigenetic modification of p53 and its binding to the promoter chromatin. Mitomycin 0-9 tumor protein p53 Homo sapiens 70-73 18647660-0 2008 Differential expression of TP53 associated genes in Fanconi anemia cells after mitomycin C and hydroxyurea treatment. Mitomycin 79-90 tumor protein p53 Homo sapiens 27-31 18647660-8 2008 The MMC induced damage was correlated with a general increase in expression of TP53-modulated DNA damage stress response genes involved in processes such as DNA repair, cell cycle progression, and apoptosis. Mitomycin 4-7 tumor protein p53 Homo sapiens 79-83 18806879-10 2008 CONCLUSIONS: These results indicate that mitomycin-induced cellular apoptosis in corneal endothelial cells may be mediated through caspase-8, caspase-9, and the mitochondrial regulated pathways as well as through upregulation of p53-dependent and p21-dependent signal transduction pathways. Mitomycin 41-50 tumor protein p53 Homo sapiens 229-232 18224251-4 2008 In primary fibroblasts with mutations in the core complex FANCA protein, we discovered that basal expression and phosphorylation of ATM (ataxia telangiectasia mutated) and p53 induced by irradiation (IR) or mitomycin C (MMC) were upregulated. Mitomycin 207-218 tumor protein p53 Homo sapiens 172-175 18559532-4 2008 In this study, we show that Tax sensitizes p53-mutant cells to a broad range of DNA-damaging agents, including mitomycin C, a bifunctional alkylator, etoposide, a topoisomerase II drug, and UV light, but not ionizing radiation, a double-strand break agent, or vinblastine, a tubulin poison. Mitomycin 111-122 tumor protein p53 Homo sapiens 43-46 18224251-4 2008 In primary fibroblasts with mutations in the core complex FANCA protein, we discovered that basal expression and phosphorylation of ATM (ataxia telangiectasia mutated) and p53 induced by irradiation (IR) or mitomycin C (MMC) were upregulated. Mitomycin 220-223 tumor protein p53 Homo sapiens 172-175 18202783-3 2008 The data obtained show that normal human lymphocytes exposed in vitro to known DNA-damaging agents, e.g. H2O2, ionizing radiation and mitomycin C, exhibit an asynchronous replication of the genes TP53 and RB1. Mitomycin 134-145 tumor protein p53 Homo sapiens 196-200 17530733-0 2007 Mitomycin-DNA adducts induce p53-dependent and p53-independent cell death pathways. Mitomycin 0-9 tumor protein p53 Homo sapiens 29-32 17530733-0 2007 Mitomycin-DNA adducts induce p53-dependent and p53-independent cell death pathways. Mitomycin 0-9 tumor protein p53 Homo sapiens 47-50 17530733-5 2007 In cell lines lacking wild-type p53, DMC was reproducibly more cytotoxic than MC, but it generated barely detectable signal transduction markers associated with apoptotic death. Mitomycin 38-40 tumor protein p53 Homo sapiens 32-35 17530733-8 2007 In cell lines with a functional p53 pathway, both MC and DMC induced apoptosis. Mitomycin 50-52 tumor protein p53 Homo sapiens 32-35 17530733-9 2007 In the presence of p53, both MC and DMC activate procaspases; however, the spectrum of procaspases involved differs for the two drugs, as does induction of p73. Mitomycin 29-31 tumor protein p53 Homo sapiens 19-22 15908423-4 2005 Nuclear accumulation of p53 protein in mdm2 SNP309 cells results after 6 h of camptothecin, etoposide, or mitomycin C treatment, with the p53 protein phosphorylated at Ser15. Mitomycin 106-117 tumor protein p53 Homo sapiens 24-27 16019139-6 2006 MMC treatment induced a reduction in the expressions of the E6 oncogene and IL-18, in a p53-independent manner. Mitomycin 0-3 tumor protein p53 Homo sapiens 88-91 16186332-8 2005 Treatment with mitomycin-C resulted in the increased expression of Fas, FasL, Bad, and phosphorylated p53 and a decreased level of phosphorylated AKT. Mitomycin 15-26 tumor protein p53 Homo sapiens 102-105 17372198-2 2007 We have investigated the effect of p53 activation on the proteome using 2D gel electrophoresis analysis of mitomycin C-treated HCT116 colon carcinoma cells carrying wild-type p53. Mitomycin 107-118 tumor protein p53 Homo sapiens 35-38 17372198-2 2007 We have investigated the effect of p53 activation on the proteome using 2D gel electrophoresis analysis of mitomycin C-treated HCT116 colon carcinoma cells carrying wild-type p53. Mitomycin 107-118 tumor protein p53 Homo sapiens 175-178 15774934-13 2005 p53 as an antiproliferative drug has the potential to replace mitomycin C and 5-fluorouracil in glaucoma surgery. Mitomycin 62-73 tumor protein p53 Homo sapiens 0-3 11585319-8 2001 We further obtained evidence of the upregulation of the intracellular apoptotic signalling cascade, represented by bcl-2 and bax, the transcription factor p53 and the active form of caspase 3, after pretreatment with mitomycin C. Mitomycin 217-228 tumor protein p53 Homo sapiens 155-158 15608686-5 2005 Similarly, constitutive hTERT expression inhibited wild-type p53-dependent apoptosis in response to mitomycin C or 5-fluorouracil in HCT116 colon carcinoma cells carrying endogenous p53. Mitomycin 100-111 tumor protein p53 Homo sapiens 61-64 15208667-4 2004 We have studied here the p53 response to DNA-damaging agents (camptothecin, mitomycin C) in individual cells. Mitomycin 76-87 tumor protein p53 Homo sapiens 25-28 14654539-0 2003 TP53 gene mutations predict the response to neoadjuvant treatment with 5-fluorouracil and mitomycin in locally advanced breast cancer. Mitomycin 90-99 tumor protein p53 Homo sapiens 0-4 14654539-6 2003 CONCLUSION: This study revealed a significant association between lack of response to 5-fluorouracil and mitomycin and mutations affecting the L2/L3 domains of the p53 protein. Mitomycin 105-114 tumor protein p53 Homo sapiens 164-167 12468545-5 2003 After treatment with Vp16 or mitomycin C, control cells underwent apoptosis in a p53-dependent manner; however, overexpression of catalase inhibited this apoptosis. Mitomycin 29-40 tumor protein p53 Homo sapiens 81-84 12468545-6 2003 Basal levels as well as Vp16- or mitomycin C-stimulated levels of p53 and p21 protein were decreased in the catalase-overexpressing cells as compared with control cells; however, p53 mRNA levels were not decreased by catalase. Mitomycin 33-44 tumor protein p53 Homo sapiens 66-69 15183489-0 2004 P53-independent thermosensitization by mitomycin C in human non-small-cell lung cancer cells. Mitomycin 39-50 tumor protein p53 Homo sapiens 0-3 15183489-1 2004 PURPOSE: To elucidate the relationship between p53 functions and the interactive effects of the combined treatment with mild hyperthermia and mitomycin C. Mitomycin 142-153 tumor protein p53 Homo sapiens 47-50 15183489-9 2004 CONCLUSION: Our findings demonstrate a p53-independent mechanism for an interactively cytotoxic enhancement by combined treatment with mild hyperthermia and mitomycin C. Mitomycin 157-168 tumor protein p53 Homo sapiens 39-42 15199132-3 2004 Activation of p53 by the DNA damaging agent mitomycin C (MC) was accompanied by a potent repression of CAIX expression and the CA9 promoter in MCF-7 but not in Saos-2 cells. Mitomycin 44-55 tumor protein p53 Homo sapiens 14-17 15199132-3 2004 Activation of p53 by the DNA damaging agent mitomycin C (MC) was accompanied by a potent repression of CAIX expression and the CA9 promoter in MCF-7 but not in Saos-2 cells. Mitomycin 57-59 tumor protein p53 Homo sapiens 14-17 15199132-6 2004 Similarly, CA9 promoter activity was downregulated by MC in HCT 116 p53(+/+) but not the isogenic p53(-/-) cells. Mitomycin 54-56 tumor protein p53 Homo sapiens 68-71 12807744-6 2003 Furthermore, caffeine also inhibited the accumulation of p53 by a variety of stress-inducing agents in vivo, such as 5-fluorouracil, doxorubicin, mitomycin C, camptothecin and roscovitine. Mitomycin 146-157 tumor protein p53 Homo sapiens 57-60 11997093-5 2002 Expression of CDM2 was shown to be transcriptionally upregulated in the primary CEF cells where p53 was activated by either mitomycin C treatment or by the exogenous transfection of the chicken p53 cDNA. Mitomycin 124-135 tumor protein p53 Homo sapiens 96-99 11562347-3 2001 Dexamethasone (Dex) stimulates the degradation of endogenous GR and p53 by the proteasome pathway in HUVEC under hypoxia and mitomycin C treatments, and also in hepatoma cells (HepG2) under normoxia. Mitomycin 125-136 tumor protein p53 Homo sapiens 68-71 11602059-7 2001 Cytotoxicity assays revealed that the wt-p53 transfectants were more sensitive to doxorubicin and mitomycin compared with the pNeo transformants. Mitomycin 98-107 tumor protein p53 Homo sapiens 41-44 11706756-2 2001 The aim of this study was to determine the predictive value of p53 mutation or the expression of GML, a target of p53, for sensitivity to 5-FU and MMC. Mitomycin 147-150 tumor protein p53 Homo sapiens 63-66 11706756-2 2001 The aim of this study was to determine the predictive value of p53 mutation or the expression of GML, a target of p53, for sensitivity to 5-FU and MMC. Mitomycin 147-150 tumor protein p53 Homo sapiens 114-117 11706756-9 2001 CONCLUSION: GML expression and p53 mutation in colorectal cancer may be useful predictive genetic markers for sensitivity to MMC and 5-FU, respectively. Mitomycin 125-128 tumor protein p53 Homo sapiens 31-34 11313875-5 2001 Nuclear accumulation of p53 was induced in NB cells using substances which disturb p53"s tertiary structure at its zinc finger motif, or by treatment with mitomycin C. Mitomycin 155-166 tumor protein p53 Homo sapiens 24-27 11313875-7 2001 Even though p53 showed DNA-binding capability after mitomycin C treatment of NB cells, the target gene products MDM2 and p21(WAF1,CIP1,SDI1) were not synthesized and no p53 transactivating activity measured in a reporter gene assay. Mitomycin 52-63 tumor protein p53 Homo sapiens 12-15 11462153-11 2001 Western blot analysis of p53 and p21 revealed a gradual increase in the level of these proteins when RPE cells were exposed to increasing concentrations of MMC. Mitomycin 156-159 tumor protein p53 Homo sapiens 25-28 10189126-10 1999 Among those patients whose tumors overexpressed p53, there was a trend toward improved outcome in the arm that received 5-FU and mitomycin-C compared with the arm that received 5-FU only. Mitomycin 129-140 tumor protein p53 Homo sapiens 48-51 11223035-3 2001 In this report, the DNA alkylating agents mitomycin C (MMC) and methylmethane sulfonate (MMS), as well as UV radiation, stabilized p53 in a manner independent of phosphorylation in p53 N-terminus. Mitomycin 42-53 tumor protein p53 Homo sapiens 131-134 11223035-3 2001 In this report, the DNA alkylating agents mitomycin C (MMC) and methylmethane sulfonate (MMS), as well as UV radiation, stabilized p53 in a manner independent of phosphorylation in p53 N-terminus. Mitomycin 55-58 tumor protein p53 Homo sapiens 131-134 11172593-5 2001 Upon DNA damage by treatment with mitomycin C the DNA-binding activity was increased, as known for cells with wild-type p53. Mitomycin 34-45 tumor protein p53 Homo sapiens 120-123 11299739-6 2001 We therefore concluded that immunohistochemical studies for p53 and p21 were useful for predicting the chemosensitivities of colon and gastric cancer to MMC and 5-FU. Mitomycin 153-156 tumor protein p53 Homo sapiens 60-63 11405176-0 2001 Mitomycin C and cisplatin enhanced the antitumor activity of p53-expressing adenovirus in cervical cancer cells. Mitomycin 0-11 tumor protein p53 Homo sapiens 61-64 10884389-2 2000 In this study, we show that BRCA1 is initially up-regulated, followed by a reduction to below basal levels in response to treatment with the DNA-damaging agents adriamycin and mitomycin C, and that the reduction of BRCA1 expression is dependent on the presence of wild-type p53. Mitomycin 176-187 tumor protein p53 Homo sapiens 274-277 10842327-7 2000 P53 induction occurred in HPV-16 E6 and HPV-16 E6/E7 expressing cells after exposure to cisplatin or MMC, though never to levels found in normal untreated HKCs. Mitomycin 101-104 tumor protein p53 Homo sapiens 0-3 10760566-3 2000 Upregulation of endogenous p53 by mitomycin C treatment in MaTu cells also had a profound effect on MN expression as well as the activity of MN promoter in a reporter construct. Mitomycin 34-45 tumor protein p53 Homo sapiens 27-30 10699952-0 2000 UCN-01 selectively enhances mitomycin C cytotoxicity in p53 defective cells which is mediated through S and/or G(2) checkpoint abrogation. Mitomycin 28-39 tumor protein p53 Homo sapiens 56-59 10699952-3 2000 In this study, we report that UCN-01 selectively enhances the cytotoxicity of MMC in human p53 mutant cell lines. Mitomycin 78-81 tumor protein p53 Homo sapiens 91-94 10699952-6 2000 In p53 wild-type MCF-7 breast carcinoma cells, the cyclin-dependent kinase inhibitor protein p21/WAF1 was markedly induced after the treatment with MMC alone, although this response was significantly delayed from the time of MMC treatment. Mitomycin 148-151 tumor protein p53 Homo sapiens 3-6 10699952-6 2000 In p53 wild-type MCF-7 breast carcinoma cells, the cyclin-dependent kinase inhibitor protein p21/WAF1 was markedly induced after the treatment with MMC alone, although this response was significantly delayed from the time of MMC treatment. Mitomycin 225-228 tumor protein p53 Homo sapiens 3-6 10699952-7 2000 Detailed cell-cycle studies revealed that UCN-01 abrogated S and G(2) phase accumulation induced by MMC in p53 defective cells and to a lesser extent in p53 wild-type cell lines. Mitomycin 100-103 tumor protein p53 Homo sapiens 107-110 10741907-10 2000 Meanwhile, Ad-p53 gene transfer combined with taxol, cisplatin, doxorubicin or mitomycin C was shown to be even more effective in suppressing growth in the two cell lines. Mitomycin 79-90 tumor protein p53 Homo sapiens 14-17 9506540-3 1998 When p53 was expressed at sublethal levels, it sensitized cells to the DNA-damaging drugs Adriamycin, mitomycin C, actinomycin D, etoposide (VP16), cisplatin and CPT11. Mitomycin 102-113 tumor protein p53 Homo sapiens 5-8 9212237-8 1997 Treatment of both cell lines with mitomycin C (MMC), which acts with a mechanism different from CDDP, caused equal accumulation of p53 and induction of bax. Mitomycin 34-45 tumor protein p53 Homo sapiens 131-134 9285062-7 1997 The results show that MMC treatment inhibited sod1 gene transcription through p53-mediated transcriptional repression. Mitomycin 22-25 tumor protein p53 Homo sapiens 78-81 9212237-8 1997 Treatment of both cell lines with mitomycin C (MMC), which acts with a mechanism different from CDDP, caused equal accumulation of p53 and induction of bax. Mitomycin 47-50 tumor protein p53 Homo sapiens 131-134 8945622-4 1996 When exposed to DNA-damaging agents, cisplatin or mitomycin C, apoptosis was induced in RT4 with the wild-type (wt) p53/wt p21, whereas T24 with the p53 non-sense mutation/wt p21 was resistant. Mitomycin 50-61 tumor protein p53 Homo sapiens 116-119 8945622-4 1996 When exposed to DNA-damaging agents, cisplatin or mitomycin C, apoptosis was induced in RT4 with the wild-type (wt) p53/wt p21, whereas T24 with the p53 non-sense mutation/wt p21 was resistant. Mitomycin 50-61 tumor protein p53 Homo sapiens 149-152 8707413-8 1996 Ad-p53-infected SKBr3 breast cancer cells were more sensitive to cytotoxicity of the DNA damaging drugs mitomycin C or Adriamycin, but not the M-phase specific drug vincristine. Mitomycin 104-115 tumor protein p53 Homo sapiens 3-6 8704210-8 1996 To analyze the possible interaction of FAC with the p53 pathway, we analyzed p53 induction in mock and corrected cell lines following exposure to MMC. Mitomycin 146-149 tumor protein p53 Homo sapiens 77-80 8707413-9 1996 Our results suggest that Ad-p53 is capable of infecting and killing cancer cells of diverse tissue origins (including multi-drug resistant cancer cells), that p21WAFI/CIPI may be a useful marker of p53 infectivity and that there may be synergy between Ad-p53 and either mitomycin C or Adriamycin induced cell death in tumors with p53 mutations. Mitomycin 270-281 tumor protein p53 Homo sapiens 28-31 7896881-4 1995 Upon introduction of temperature-sensitive p53 into HC11 cells, which lack wild-type (wt) p53, PCD was observed after mitomycin treatment at 32 degrees, when the ts p53 protein is in wt conformation. Mitomycin 118-127 tumor protein p53 Homo sapiens 43-46 8639538-1 1996 The tumor suppressor protein p53 plays a central role in the cellular response to genotoxic lesions and has been shown to be activated by most anticancer agents such as mitomycin C. Mitomycin 169-180 tumor protein p53 Homo sapiens 29-32 7478558-5 1995 Previous transfection of linear or circular, single- or ds, DNA, followed by mitomycin C-treatment, lead to a dramatic increase in nuclear p53 accumulation and p53 activity according to electrophoretic mobility shift analysis. Mitomycin 77-88 tumor protein p53 Homo sapiens 139-142 7478558-5 1995 Previous transfection of linear or circular, single- or ds, DNA, followed by mitomycin C-treatment, lead to a dramatic increase in nuclear p53 accumulation and p53 activity according to electrophoretic mobility shift analysis. Mitomycin 77-88 tumor protein p53 Homo sapiens 160-163 7644500-9 1995 In contrast, two HPV immortalized cell lines in which p53 protein was destroyed by E6-modulated ubiquitinylation were highly sensitive to apoptosis induced by MMC. Mitomycin 159-162 tumor protein p53 Homo sapiens 54-57 7644500-12 1995 Thus, HPV 16E6 can sensitize mammary epithelial cells to MMC-induced apoptosis via a p53- and p21-independent pathway. Mitomycin 57-60 tumor protein p53 Homo sapiens 85-88 7623839-2 1995 We show that exposure of cells to various genotoxic agents, including anticancer drugs such as mitomycin and 5-fluorouracil, results in an increase in p53 mRNA levels and in p53 promoter activation, indicating that the p53 genotoxic stress response is partly regulated at the transcriptional level. Mitomycin 95-104 tumor protein p53 Homo sapiens 151-154 7623839-2 1995 We show that exposure of cells to various genotoxic agents, including anticancer drugs such as mitomycin and 5-fluorouracil, results in an increase in p53 mRNA levels and in p53 promoter activation, indicating that the p53 genotoxic stress response is partly regulated at the transcriptional level. Mitomycin 95-104 tumor protein p53 Homo sapiens 174-177 7623839-2 1995 We show that exposure of cells to various genotoxic agents, including anticancer drugs such as mitomycin and 5-fluorouracil, results in an increase in p53 mRNA levels and in p53 promoter activation, indicating that the p53 genotoxic stress response is partly regulated at the transcriptional level. Mitomycin 95-104 tumor protein p53 Homo sapiens 174-177 7750085-1 1995 Anticancer drugs etoposide and mitomycin C increased nuclear p53 protein and decreased proliferating cell nuclear antigen (PCNA) of PLC/PRF/5 human hepatoma cells. Mitomycin 31-42 tumor protein p53 Homo sapiens 61-64 7896881-5 1995 Thus, wt p53 mediates activation of PCD in response to mitomycin in HC11 cells. Mitomycin 55-64 tumor protein p53 Homo sapiens 9-12 7824283-7 1995 Moreover, the same impairment in p53 induction is observed after exposure to mitomycin C, a chemical agent for which FA cells demonstrate a specific cellular and chromosomal hypersensitivity, as well as after u.v.-B irradiation, an agent known to cause oxidative stress. Mitomycin 77-88 tumor protein p53 Homo sapiens 33-36 34624459-6 2021 The knockdown of p53, a downstream effector of GSK3beta and an important regulator of cell senescence, repressed mitomycin-induced alveolar epithelial cell senescence. Mitomycin 113-122 tumor protein p53 Homo sapiens 17-20 8084605-0 1994 p56/p53lyn tyrosine kinase activation in mammalian cells treated with mitomycin C. Mitomycin 70-81 tumor protein p53 Homo sapiens 4-7 8485705-2 1993 Activation of p53-DNA binding was seen for treatment with radiation, hydrogen peroxide, actinomycin D, Adriamycin, etoposide, camptothecin, 5-fluorouracil, mitomycin C, and cisplatin. Mitomycin 156-167 tumor protein p53 Homo sapiens 14-17 33567038-8 2021 The apoptotic rates (p=0.002) of mitomycin C treated basal cell carcinoma were higher than those of the other treated cells, and their TP53 was significantly upregulated (p=0.0001). Mitomycin 33-44 tumor protein p53 Homo sapiens 135-139