PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17080554-7 2006 These results suggest that EGCG may have an inhibitory effect on UVB-induced photo-damage and apoptosis by blocking the cytokine secretion and the mRNA expressions of p53, p21 and c-fos genes. epigallocatechin gallate 27-31 tumor protein p53 Homo sapiens 167-170 15764647-1 2005 Treatment with epigallocatechin-3-gallate (EGCG), a polyphenolic compound of green tea, results in activation of p53 and induction of apoptosis in prostate cancer LnCaP cells. epigallocatechin gallate 15-41 tumor protein p53 Homo sapiens 113-116 16157026-6 2005 RT-PCR method was employed to detect the influence of EGCG on the expressions of hTERT, c-myc, p53 and mad1 genes in sensitive cancer cell line. epigallocatechin gallate 54-58 tumor protein p53 Homo sapiens 95-98 16157026-11 2005 After EGCG administration, the expression of hTERT and c-myc genes in MKN45 cells was decreased, that of the mad1 gene increased, and that of the p53 gene unchanged. epigallocatechin gallate 6-10 tumor protein p53 Homo sapiens 146-149 15764647-1 2005 Treatment with epigallocatechin-3-gallate (EGCG), a polyphenolic compound of green tea, results in activation of p53 and induction of apoptosis in prostate cancer LnCaP cells. epigallocatechin gallate 43-47 tumor protein p53 Homo sapiens 113-116 15764647-2 2005 However, no direct evidence has delineated the role of p53 and p53-dependent pathways in EGCG-mediated apoptosis. epigallocatechin gallate 89-93 tumor protein p53 Homo sapiens 63-66 15764647-4 2005 Treatment of the resultant cells, PC3-p53, with EGCG led to, as reported earlier in LnCaP cells, an increase in p53 protein, which exacerbated both G1 arrest and apoptosis. epigallocatechin gallate 48-52 tumor protein p53 Homo sapiens 38-41 15764647-4 2005 Treatment of the resultant cells, PC3-p53, with EGCG led to, as reported earlier in LnCaP cells, an increase in p53 protein, which exacerbated both G1 arrest and apoptosis. epigallocatechin gallate 48-52 tumor protein p53 Homo sapiens 112-115 15764647-6 2005 The cells lacking p53 continued to cycle and did not undergo apoptosis upon treatment with similar concentrations of EGCG, thus establishing the action of EGCG in a p53-dependent manner. epigallocatechin gallate 155-159 tumor protein p53 Homo sapiens 18-21 15764647-6 2005 The cells lacking p53 continued to cycle and did not undergo apoptosis upon treatment with similar concentrations of EGCG, thus establishing the action of EGCG in a p53-dependent manner. epigallocatechin gallate 155-159 tumor protein p53 Homo sapiens 165-168 15764647-8 2005 Inactivation of p53 using small interfering RNA (siRNA) rendered these cells resistant to EGCG-mediated apoptosis. epigallocatechin gallate 90-94 tumor protein p53 Homo sapiens 16-19 15764647-13 2005 In summary, using isogenic cell lines and siRNA, we have clearly demonstrated that EGCG activates growth arrest and apoptosis primarily via p53-dependent pathway that involves the function of both p21 and Bax such that down-regulation of either molecule confers a growth advantage to the cells. epigallocatechin gallate 83-87 tumor protein p53 Homo sapiens 140-143 15795422-6 2005 Micromolar (-)epigallocatechin gallate and quercetin partially eliminated the dichlorodihydrofluorescein (DCF) and phospho-p53 staining, suggesting that these flavonoids inhibited the accumulation of intracellular oxidants and nuclear transactivation of p53 in H2O2-exposed cells. epigallocatechin gallate 11-38 tumor protein p53 Homo sapiens 123-126 15795422-6 2005 Micromolar (-)epigallocatechin gallate and quercetin partially eliminated the dichlorodihydrofluorescein (DCF) and phospho-p53 staining, suggesting that these flavonoids inhibited the accumulation of intracellular oxidants and nuclear transactivation of p53 in H2O2-exposed cells. epigallocatechin gallate 11-38 tumor protein p53 Homo sapiens 254-257 20368822-9 2004 The continual expression in p21WAF1 suggests that EGCG acts in the same way with p53 proteins to facilitate apoptosis after EGCG treatment. epigallocatechin gallate 124-128 tumor protein p53 Homo sapiens 81-84 15657356-0 2005 Epigallocatechin-3-gallate induces apoptosis in estrogen receptor-negative human breast carcinoma cells via modulation in protein expression of p53 and Bax and caspase-3 activation. epigallocatechin gallate 0-26 tumor protein p53 Homo sapiens 144-147 15657356-5 2005 Induction of apoptosis by EGCG could be corroborated to the increased expression of tumor suppressor protein p53 and its phosphorylation at Ser 15 residue. epigallocatechin gallate 26-30 tumor protein p53 Homo sapiens 109-112 15350370-10 2004 The continual expression in p21WAF1 suggests that EGCG acts in the same way with p53 proteins to facilitate apoptosis after EGCG treatment. epigallocatechin gallate 124-128 tumor protein p53 Homo sapiens 81-84 12586742-6 2003 Treatment with 80 microg/ml EGCG induced the tumor suppressor p53, which was functional as judged by activation of the target cyclin-dependent kinase inhibitor p21CIP1. epigallocatechin gallate 28-32 tumor protein p53 Homo sapiens 62-65 12894226-0 2003 Role of p53 and NF-kappaB in epigallocatechin-3-gallate-induced apoptosis of LNCaP cells. epigallocatechin gallate 29-55 tumor protein p53 Homo sapiens 8-11 12894226-3 2003 In the present study, we report that EGCG-induced apoptosis in human prostate carcinoma LNCaP cells is mediated via modulation of two related pathways: (a) stabilization of p53 by phosphorylation on critical serine residues and p14ARF-mediated downregulation of murine double minute 2(MDM2) protein, and (b) negative regulation of NF-kappaB activity, thereby decreasing the expression of the proapoptotic protein Bcl-2. epigallocatechin gallate 37-41 tumor protein p53 Homo sapiens 173-176 12894226-4 2003 EGCG-induced stabilization of p53 caused an upregulation in its transcriptional activity, thereby resulting in activation of its downstream targets p21/WAF1 and Bax. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 30-33 12894226-5 2003 Thus, EGCG had a concurrent effect on two important transcription factors p53 and NF-kappaB, causing a change in the ratio of Bax/Bcl-2 in a manner that favors apoptosis. epigallocatechin gallate 6-10 tumor protein p53 Homo sapiens 74-77 12586742-10 2003 Thus, EGCG inhibits growth and induces death of SMCs in a p53- and NF-kappaB-dependent manner. epigallocatechin gallate 6-10 tumor protein p53 Homo sapiens 58-61 10462699-9 1999 EGCG also induced the expression of the Cdk inhibitor p21 protein and this effect correlated with the increase in p53 levels. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 114-117 12595758-0 2003 Green tea constituent (-)-epigallocatechin-3-gallate inhibits Hep G2 cell proliferation and induces apoptosis through p53-dependent and Fas-mediated pathways. epigallocatechin gallate 22-52 tumor protein p53 Homo sapiens 118-121 12595758-5 2003 ELISA showed that EGCG significantly increased the expression of p53 and p21/WAF1 protein, and this contributed to cell cycle arrest. epigallocatechin gallate 18-22 tumor protein p53 Homo sapiens 65-68 12595758-7 2003 Taken together, our study suggests that the induction of p53 and the activity of the Fas/FasL apoptotic system play major roles in the antiproliferative activity of EGCG in Hep G2 cells. epigallocatechin gallate 165-169 tumor protein p53 Homo sapiens 57-60 10739747-11 2000 Western blot analysis revealed that EGCG treatment resulted in (i) a dose-dependent increase of p53 in LNCaP cells (carrying wild-type p53), but not in DU145 cells (carrying mutant p53), and (ii) induction of cyclin kinase inhibitor WAF1/p21 in both cell types. epigallocatechin gallate 36-40 tumor protein p53 Homo sapiens 96-99 10739747-11 2000 Western blot analysis revealed that EGCG treatment resulted in (i) a dose-dependent increase of p53 in LNCaP cells (carrying wild-type p53), but not in DU145 cells (carrying mutant p53), and (ii) induction of cyclin kinase inhibitor WAF1/p21 in both cell types. epigallocatechin gallate 36-40 tumor protein p53 Homo sapiens 135-138 10739747-11 2000 Western blot analysis revealed that EGCG treatment resulted in (i) a dose-dependent increase of p53 in LNCaP cells (carrying wild-type p53), but not in DU145 cells (carrying mutant p53), and (ii) induction of cyclin kinase inhibitor WAF1/p21 in both cell types. epigallocatechin gallate 36-40 tumor protein p53 Homo sapiens 135-138 10739747-12 2000 These results suggest that EGCG negatively modulates PCA cell growth, by affecting mitogenesis as well as inducing apoptosis, in cell-type-specific manner which may be mediated by WAF1/p21-caused G(0)/G(1)-phase cell-cycle arrest, irrespective of the androgen association or p53 status of the cells. epigallocatechin gallate 27-31 tumor protein p53 Homo sapiens 275-278 34944489-7 2021 We found that EGCG (50 muM) significantly inhibited the aggregation of (i)sAPPbetaf, blocked p-TAU, increased Psim, decreased oxidation of DJ-1 at residue Cys106-SH, and inhibited the activation of transcription factor c-JUN and P53, PUMA, and CASPASE-3 in mutant ChLNs compared to WT. epigallocatechin gallate 14-18 tumor protein p53 Homo sapiens 230-233 10190556-11 1999 Mutations seen similarly in the human Ki-ras codon 12 or p53 codons 157, 248, and 273 of lung tumor were also found in the rpsL gene, and the mutations were suppressed by the EGCG treatment. epigallocatechin gallate 175-179 tumor protein p53 Homo sapiens 57-60 34945706-5 2021 GTE selectively targeted breast tumor cells without cytotoxic effect on non-tumoral cells and p53 inhibition led to an increase in viable cells, especially in MCF-7, suggesting the involvement of p53 in GTE-induced cytotoxicity. epigallocatechin gallate 203-206 tumor protein p53 Homo sapiens 94-97 34945706-5 2021 GTE selectively targeted breast tumor cells without cytotoxic effect on non-tumoral cells and p53 inhibition led to an increase in viable cells, especially in MCF-7, suggesting the involvement of p53 in GTE-induced cytotoxicity. epigallocatechin gallate 203-206 tumor protein p53 Homo sapiens 196-199 34945706-7 2021 An increment in p53 and p21 expression stimulated by GTE was observed in MCF-7, and the opposite phenomenon was found in MDA-MB-231 cells, with a redistribution of mutant-p53 from the nucleus and no differences in p21 levels. epigallocatechin gallate 53-56 tumor protein p53 Homo sapiens 16-19 34945706-7 2021 An increment in p53 and p21 expression stimulated by GTE was observed in MCF-7, and the opposite phenomenon was found in MDA-MB-231 cells, with a redistribution of mutant-p53 from the nucleus and no differences in p21 levels. epigallocatechin gallate 53-56 tumor protein p53 Homo sapiens 171-174 34590505-8 2021 On a genetic basis, both agents engaged the BCL-2 family-regulated and caspase-dependent intrinsic apoptotic pathway, but EGCG and HNK triggered apoptosis via p53-independent and p53-dependent pathways, respectively. epigallocatechin gallate 122-126 tumor protein p53 Homo sapiens 159-162 34799573-5 2021 The results of this approach closely reproduce the experimental data from recent literature on the binding of the ligand epigallocatechin gallate (EGCG) to the intrinsically disordered N-terminal domain of the tumor suppressor p53. epigallocatechin gallate 121-145 tumor protein p53 Homo sapiens 227-230 34799573-5 2021 The results of this approach closely reproduce the experimental data from recent literature on the binding of the ligand epigallocatechin gallate (EGCG) to the intrinsically disordered N-terminal domain of the tumor suppressor p53. epigallocatechin gallate 147-151 tumor protein p53 Homo sapiens 227-230 34590505-8 2021 On a genetic basis, both agents engaged the BCL-2 family-regulated and caspase-dependent intrinsic apoptotic pathway, but EGCG and HNK triggered apoptosis via p53-independent and p53-dependent pathways, respectively. epigallocatechin gallate 122-126 tumor protein p53 Homo sapiens 179-182 33425912-12 2020 EGCG enhanced the anti-tumor effect of DOX in bladder cancer via NF-kappaB/MDM2/p53 pathway, suggesting the potential clinical application against bladder cancer patients. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 80-83 35548580-5 2022 Moreover, it was also found that SIRT1 is down-regulated by EGCG, and the SIRT1-p53 signaling pathway participates in the effects of EGCG on CNE-2 and 5-8 F cells. epigallocatechin gallate 133-137 tumor protein p53 Homo sapiens 80-83 35548580-6 2022 Taken together, the findings of this study provided evidence that EGCG could inhibit the growth of NPC cell lines and is linked with the inhibition of the SIRT1-p53 signaling pathway, suggesting the therapeutic potential of EGCG in human NPC. epigallocatechin gallate 66-70 tumor protein p53 Homo sapiens 161-164 35548580-6 2022 Taken together, the findings of this study provided evidence that EGCG could inhibit the growth of NPC cell lines and is linked with the inhibition of the SIRT1-p53 signaling pathway, suggesting the therapeutic potential of EGCG in human NPC. epigallocatechin gallate 224-228 tumor protein p53 Homo sapiens 161-164 33918387-0 2021 Distinct Classes of Flavonoids and Epigallocatechin Gallate, Polyphenol Affects an Oncogenic Mutant p53 Protein, Cell Growth and Invasion in a TNBC Breast Cancer Cell Line. epigallocatechin gallate 35-59 tumor protein p53 Homo sapiens 100-103 33906321-0 2021 Epigallocatechin Gallate Enhances Inhibition Effect of DDP on the Proliferation of Gastric Cancer BGC-823 Cells by Regulating p19Arf-p53-p21Cip1 Signaling Pathway. epigallocatechin gallate 0-24 tumor protein p53 Homo sapiens 133-136 33906321-10 2021 EGCG combined with DDP treatment caused cell cycle arrest in G1 phase in BGC-823 cells, increase of apoptosis (21.3%) vs EGCG (7.25%) and DDP (3.86%) single-use group (p <0.01), up-regulated gene and protein expressions of p19Arf, p53, p21Cip1 (p <0.01). epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 231-234 33906321-11 2021 CONCLUSION: EGCG can enhance the effect of DDP on inhibiting BGC-823 cell proliferation and inducing apoptosis via activating the p19Arf-p53-p21Cip1 signaling pathway. epigallocatechin gallate 12-16 tumor protein p53 Homo sapiens 137-140 33579943-0 2021 EGCG binds intrinsically disordered N-terminal domain of p53 and disrupts p53-MDM2 interaction. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 57-60 33579943-0 2021 EGCG binds intrinsically disordered N-terminal domain of p53 and disrupts p53-MDM2 interaction. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 74-77 33579943-2 2021 Using SPR and NMR, here we report a direct, muM interaction between EGCG and the tumor suppressor p53 (KD = 1.6 +- 1.4 muM), with the disordered N-terminal domain (NTD) identified as the major binding site (KD = 4 +- 2 muM). epigallocatechin gallate 68-72 tumor protein p53 Homo sapiens 98-101 33579943-4 2021 The EGCG-p53 interaction disrupts p53 interaction with its regulatory E3 ligase MDM2 and inhibits ubiquitination of p53 by MDM2 in an in vitro ubiquitination assay, likely stabilizing p53 for anti-tumor activity. epigallocatechin gallate 4-8 tumor protein p53 Homo sapiens 9-12 33579943-4 2021 The EGCG-p53 interaction disrupts p53 interaction with its regulatory E3 ligase MDM2 and inhibits ubiquitination of p53 by MDM2 in an in vitro ubiquitination assay, likely stabilizing p53 for anti-tumor activity. epigallocatechin gallate 4-8 tumor protein p53 Homo sapiens 34-37 33579943-4 2021 The EGCG-p53 interaction disrupts p53 interaction with its regulatory E3 ligase MDM2 and inhibits ubiquitination of p53 by MDM2 in an in vitro ubiquitination assay, likely stabilizing p53 for anti-tumor activity. epigallocatechin gallate 4-8 tumor protein p53 Homo sapiens 34-37 33579943-4 2021 The EGCG-p53 interaction disrupts p53 interaction with its regulatory E3 ligase MDM2 and inhibits ubiquitination of p53 by MDM2 in an in vitro ubiquitination assay, likely stabilizing p53 for anti-tumor activity. epigallocatechin gallate 4-8 tumor protein p53 Homo sapiens 34-37 33579943-5 2021 Our work provides insights into the mechanisms for EGCG"s anticancer activity and identifies p53 NTD as a target for cancer drug discovery through dynamic interactions with small molecules. epigallocatechin gallate 51-55 tumor protein p53 Homo sapiens 93-96 32990229-0 2020 [Epigallocatechin gallate induces CHD5 gene demethylation to promote acute myeloid leukemia cell apoptosis in vitro by regulating p19Arf-p53-p21Cip1 signaling pathway]. epigallocatechin gallate 1-25 tumor protein p53 Homo sapiens 137-140 33425912-0 2020 EGCG Enhanced the Anti-tumor Effect of Doxorubicine in Bladder Cancer via NF-kappaB/MDM2/p53 Pathway. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 89-92 33425912-8 2020 Further mechanistic studies determined that the combination of DOX and EGCG inhibited phosphorylated NF-kappaB and MDM2 expression, and up-regulated p53 expression in tumor, as assessed by western blot and immunohistochemistry. epigallocatechin gallate 71-75 tumor protein p53 Homo sapiens 149-152 33425912-9 2020 Western blot in SW780 cells also confirmed that the combined use of EGCG and DOX caused significant increase in p53, p21, and cleaved-PARP expression, and induced significant inhibition in phosphorylated NF-kappaB and MDM2. epigallocatechin gallate 68-72 tumor protein p53 Homo sapiens 112-115 32990229-6 2020 EGCG treatment caused obvious cell cycle arrest in G1 phase, significantly increased cell apoptosis, downregulated the expression of DNMT1 and upregulated the expressions of CHD5, p19Arf, p53 and p21Cip1 in KG-1 and THP-1 cells (P < 0.05). epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 188-191 32990229-7 2020 CONCLUSIONS: EGCG reduces hypermethylation of CHD5 gene in KG-1 and THP-1 cells by downregulating DNMT1 to restore its expression, which results in upregulated expressions of p19Arf, p53 and p21Cip1 and induces cell apoptosis. epigallocatechin gallate 13-17 tumor protein p53 Homo sapiens 183-186 29940201-4 2018 EGCG markedly decreased the levels of inflammatory and oxidative stress factors including nuclear factor kappaB (NF-kappaB), tumor necrosis factor-alpha, interleukin-6, reactive oxygen species, malondialdehyde and p53 protein, and markedly increased superoxide dismutases (SOD), glutathione peroxidase and SOD2 protein. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 214-217 31029907-0 2019 Epigallocatechin gallate prevents mitochondrial impairment and cell apoptosis by regulating miR-30a/p53 axis. epigallocatechin gallate 0-24 tumor protein p53 Homo sapiens 100-103 31029907-1 2019 PURPOSE: This study was designed to investigate whether EGCG prevents cardiac I/R mitochondrial impairment and cell apoptosis by regulating miR-30a/p53 axis. epigallocatechin gallate 56-60 tumor protein p53 Homo sapiens 148-151 31029907-11 2019 The beneficial effect of EGCG was associated with restored levels of miR-30a expression in the I/R injury that correspond to p53 mRNA downregulation. epigallocatechin gallate 25-29 tumor protein p53 Homo sapiens 125-128 31029907-13 2019 More importantly, EGCG pretreatment inhibited the expression of mitochondrial apoptotic related proteins downstream of the miR-30a/p53 pathway. epigallocatechin gallate 18-22 tumor protein p53 Homo sapiens 131-134 31029907-14 2019 CONCLUSION: This study demonstrated that EGCG pretreatment may attenuate mitochondrial impairment and myocardial apoptosis by regulation of miR-30a/p53 axis. epigallocatechin gallate 41-45 tumor protein p53 Homo sapiens 148-151 30456590-7 2019 Presence of EGCG (50 and 100 muM) showed significant downregulation of PI3K/Akt/mTOR and AMPK signaling along with the suppression of ROS, iNOS, Cox-2, NF-kappaB, SASP and p53 mediated cell cycle inhibition in preadipocytes. epigallocatechin gallate 12-16 tumor protein p53 Homo sapiens 172-175 31797597-6 2020 Interestingly, both EGCG binding and N29K/N30D could also induce long-range structural reorganizations and lead to more compact structures that could shield key binding sites of p53-TAD regulators. epigallocatechin gallate 20-24 tumor protein p53 Homo sapiens 178-181 30513211-15 2018 On the other hand, O-EGCG induced HCT116 cells apoptosis mainly by increasing the expression of p53 and cleaved caspase-3, which might be the underlying reason why O-EGCG had stronger inhibitory effect on HCT116 cells line than EGCG. epigallocatechin gallate 21-25 tumor protein p53 Homo sapiens 96-99 27765354-9 2016 EGCG decreased mRNA and transcriptional activity of beta-catenin in p53 wild-type KB cells. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 68-71 29656126-5 2018 Quantitative reverse transcription polymerase chain reaction revealed the positive influence of EGCG on several innate immune-related genes, including IMD, proPO, QM, myosin, Rho, Rab7, p53, TNF-alpha, MAPK, and NOS, and we observed positive influences on three immune parameters, including total hemocyte count and phenoloxidase and superoxide dismutase activities, by EGCG treatment. epigallocatechin gallate 96-100 tumor protein p53 Homo sapiens 186-189 30636605-2 2018 In our previous studies, we demonstrated that p53 directly regulates Bak in mouse JB6 cells and that p53-Bak signaling axis plays an important role in mediating EGCG-induced apoptosis. epigallocatechin gallate 161-165 tumor protein p53 Homo sapiens 101-104 28927122-10 2017 The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group. epigallocatechin gallate 29-33 tumor protein p53 Homo sapiens 18-21 28927122-10 2017 The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group. epigallocatechin gallate 29-33 tumor protein p53 Homo sapiens 46-49 28927122-10 2017 The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group. epigallocatechin gallate 29-33 tumor protein p53 Homo sapiens 46-49 28927122-10 2017 The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group. epigallocatechin gallate 117-121 tumor protein p53 Homo sapiens 18-21 28927122-11 2017 The Bcl-2 expression level in the EGCG-combined si-P53 group was lower than that of the si-P53 group and higher than that of the EGCG group. epigallocatechin gallate 34-38 tumor protein p53 Homo sapiens 51-54 28927122-11 2017 The Bcl-2 expression level in the EGCG-combined si-P53 group was lower than that of the si-P53 group and higher than that of the EGCG group. epigallocatechin gallate 34-38 tumor protein p53 Homo sapiens 91-94 28247504-8 2017 Therefore, EGCG was found to promote greater cytotoxicity to BEAS-2B co-treated with BaP and BEAS-2BBaP upon gefitinib co-treatment through regulating metabolism enzymes and signaling pathways involving EGFR and p53. epigallocatechin gallate 11-15 tumor protein p53 Homo sapiens 212-215 28247504-3 2017 Co-treatment with 5 microM BaP and 20 microM EGCG in BEAS-2B promoted a significant reduction in cell viability and greater G2/M cell cycle arrest, induction of ROS, and reductions in BaP-induced CYP1A1/CYP1B1/COMT, EGFR, p-Akt (Ser473), p-p53 (Thr55), and survivin mRNA/protein expression, as well as an increase in p-p53 (Ser15). epigallocatechin gallate 45-49 tumor protein p53 Homo sapiens 240-243 28247504-3 2017 Co-treatment with 5 microM BaP and 20 microM EGCG in BEAS-2B promoted a significant reduction in cell viability and greater G2/M cell cycle arrest, induction of ROS, and reductions in BaP-induced CYP1A1/CYP1B1/COMT, EGFR, p-Akt (Ser473), p-p53 (Thr55), and survivin mRNA/protein expression, as well as an increase in p-p53 (Ser15). epigallocatechin gallate 45-49 tumor protein p53 Homo sapiens 319-322 29955703-10 2017 GEN and EGCG reduced BRCA1 CpG methylation and cell proliferation associated with increased p53. epigallocatechin gallate 8-12 tumor protein p53 Homo sapiens 92-95 25625511-9 2015 Treatment with EGCG was found to elevate the expression of p53 and p21, and eventually led to apoptosis of NPC cells via caspase 3 activation. epigallocatechin gallate 15-19 tumor protein p53 Homo sapiens 59-62 25849487-3 2015 The purpose of our in vitro study was to evaluate the impact of p53 gene silencing in conjunction with the administration of a natural compound, epigallocatechingallate (EGCG). epigallocatechin gallate 170-174 tumor protein p53 Homo sapiens 64-67 25849487-5 2015 Gene expression analysis revealed 28 genes were significantly altered (16 upregulated and 12 downregulated) in response to combined p53 siRNA and EGCG treatment. epigallocatechin gallate 146-150 tumor protein p53 Homo sapiens 132-135 27498709-6 2016 The H2O2-exposed hMSCs showed cellular senescence with significantly increased protein levels of acetyl-p53 and p21 in comparison with the untreated hMSCs, and these effects were prevented by pre-treatment with EGCG. epigallocatechin gallate 211-215 tumor protein p53 Homo sapiens 104-107 27498709-7 2016 By contrast, in Nrf2-knockdown hMSCs, EGCG lost its antioxidant effect, exhibiting high levels of acetyl-p53 and p21 following EGCG pre-treatment and H2O2 exposure. epigallocatechin gallate 38-42 tumor protein p53 Homo sapiens 105-108 27498709-8 2016 This indicates that Nrf2 and p53/p21 may be involved in the anti-senescent effect of EGCG in hMSCs. epigallocatechin gallate 85-89 tumor protein p53 Homo sapiens 29-32 24798859-8 2015 We found that (-)-epigallocatechin-3-gallate (EGCG), a constituent of green tea and a major component of the botanical drug Polyphenon E, reduced the expression of four p53-targeting miRNAs, including miR-25, miR-92, miR-141, and miR-200a. epigallocatechin gallate 14-44 tumor protein p53 Homo sapiens 170-173 24798859-8 2015 We found that (-)-epigallocatechin-3-gallate (EGCG), a constituent of green tea and a major component of the botanical drug Polyphenon E, reduced the expression of four p53-targeting miRNAs, including miR-25, miR-92, miR-141, and miR-200a. epigallocatechin gallate 46-50 tumor protein p53 Homo sapiens 170-173 25759589-4 2015 Treatment with EGCG activates the expression of the BAD, BAK, FAS, IGF1R, WNT11, and ZEB1 genes and inhibits CASP8, MYC, and TP53. epigallocatechin gallate 15-19 tumor protein p53 Homo sapiens 125-129 24179522-3 2013 EGCG treatment induced apoptosis in the presence of wild-type and mutant p53, indicating that a p53-independent pathway may contribute to EGCG-induced apoptosis in these cells. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 73-76 24712372-7 2014 These results suggested that EGCG inhibited the expression of hsa-miR-98-5p, followed by an increase of p53, thus the efficacy of cisplatin was enhanced. epigallocatechin gallate 29-33 tumor protein p53 Homo sapiens 104-107 24847310-1 2014 Physiological concentrations of the green tea extract epigallocatechin-3-gallate (EGCG) caused growth inhibition in estrogen receptor alpha (ERalpha)-positive MCF7 cells that was associated with down-regulation of the ERalpha and reduced insulin-like growth factor binding protein-2 abundance and increased protein abundance of the tumor suppressor genes p53/p21. epigallocatechin gallate 54-80 tumor protein p53 Homo sapiens 355-358 24847310-1 2014 Physiological concentrations of the green tea extract epigallocatechin-3-gallate (EGCG) caused growth inhibition in estrogen receptor alpha (ERalpha)-positive MCF7 cells that was associated with down-regulation of the ERalpha and reduced insulin-like growth factor binding protein-2 abundance and increased protein abundance of the tumor suppressor genes p53/p21. epigallocatechin gallate 82-86 tumor protein p53 Homo sapiens 355-358 24847310-4 2014 EGCG significantly increased cell death in an ERalpha-negative cell line, MDA-MB-231 that also possesses mutant p53. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 112-115 24179522-3 2013 EGCG treatment induced apoptosis in the presence of wild-type and mutant p53, indicating that a p53-independent pathway may contribute to EGCG-induced apoptosis in these cells. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 96-99 24179522-3 2013 EGCG treatment induced apoptosis in the presence of wild-type and mutant p53, indicating that a p53-independent pathway may contribute to EGCG-induced apoptosis in these cells. epigallocatechin gallate 138-142 tumor protein p53 Homo sapiens 96-99 24179522-4 2013 EGCG showed migration-suppressing effects, suggesting that this activity may also have p53-dependent and -independent components. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 87-90 24179522-5 2013 The interaction between p53 and VEGF in the EGCG-treated cells was investigated using pifithrin-alpha. epigallocatechin gallate 44-48 tumor protein p53 Homo sapiens 24-27 24179522-6 2013 Notably, the suppression of p53 activity blocked the ability of EGCG to inhibit VEGF and MMP-9 in the cells expressing wild-type p53, but not mutant p53, indicating that the effects of EGCG on VEGF may be p53-dependent or -independent. epigallocatechin gallate 64-68 tumor protein p53 Homo sapiens 28-31 24179522-6 2013 Notably, the suppression of p53 activity blocked the ability of EGCG to inhibit VEGF and MMP-9 in the cells expressing wild-type p53, but not mutant p53, indicating that the effects of EGCG on VEGF may be p53-dependent or -independent. epigallocatechin gallate 64-68 tumor protein p53 Homo sapiens 129-132 24179522-6 2013 Notably, the suppression of p53 activity blocked the ability of EGCG to inhibit VEGF and MMP-9 in the cells expressing wild-type p53, but not mutant p53, indicating that the effects of EGCG on VEGF may be p53-dependent or -independent. epigallocatechin gallate 64-68 tumor protein p53 Homo sapiens 129-132 24179522-6 2013 Notably, the suppression of p53 activity blocked the ability of EGCG to inhibit VEGF and MMP-9 in the cells expressing wild-type p53, but not mutant p53, indicating that the effects of EGCG on VEGF may be p53-dependent or -independent. epigallocatechin gallate 64-68 tumor protein p53 Homo sapiens 129-132 24179522-6 2013 Notably, the suppression of p53 activity blocked the ability of EGCG to inhibit VEGF and MMP-9 in the cells expressing wild-type p53, but not mutant p53, indicating that the effects of EGCG on VEGF may be p53-dependent or -independent. epigallocatechin gallate 185-189 tumor protein p53 Homo sapiens 28-31 23483203-0 2013 Epigallocatechin gallate promotes p53 accumulation and activity via the inhibition of MDM2-mediated p53 ubiquitination in human lung cancer cells. epigallocatechin gallate 0-24 tumor protein p53 Homo sapiens 34-37 24065519-0 2013 EGCG suppresses Fused Toes Homolog protein through p53 in cervical cancer cells. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 51-54 24065519-8 2013 p53 silencing increased the expression of FTS and also decreased the reduction in the levels of FTS expression after EGCG treatment. epigallocatechin gallate 117-121 tumor protein p53 Homo sapiens 0-3 24065519-10 2013 Collectively, these results conclude that EGCG induced anti-proliferative action in the cervical cancer cell involves reduced mRNA expression of FTS through p53. epigallocatechin gallate 42-46 tumor protein p53 Homo sapiens 157-160 24179522-1 2013 The present study investigated the regulatory mechanisms by which epigallocatechin-3-gallate (EGCG) exerts vascular endothelial growth factor (VEGF)-, p53- and AMP-activated protein kinase (AMPK)-associated pro-apoptotic and migration-suppressing effects on colon cancer cells. epigallocatechin gallate 66-92 tumor protein p53 Homo sapiens 151-154 24179522-1 2013 The present study investigated the regulatory mechanisms by which epigallocatechin-3-gallate (EGCG) exerts vascular endothelial growth factor (VEGF)-, p53- and AMP-activated protein kinase (AMPK)-associated pro-apoptotic and migration-suppressing effects on colon cancer cells. epigallocatechin gallate 94-98 tumor protein p53 Homo sapiens 151-154 23017582-5 2013 Reporter assays, using the luciferase constructs containing the NAG-1 promoter, demonstrate that p53 is required for EGCG-mediated activation of NAG-1. epigallocatechin gallate 117-121 tumor protein p53 Homo sapiens 97-100 23017582-9 2013 Taken together, these results demonstrate for the first time that EGCG induces apoptosis via ATM/p53-dependent NAG-1 expression in HNSCC, providing an additional mechanistic explanation for the apoptotic activity of EGCG. epigallocatechin gallate 66-70 tumor protein p53 Homo sapiens 97-100 23017582-9 2013 Taken together, these results demonstrate for the first time that EGCG induces apoptosis via ATM/p53-dependent NAG-1 expression in HNSCC, providing an additional mechanistic explanation for the apoptotic activity of EGCG. epigallocatechin gallate 216-220 tumor protein p53 Homo sapiens 97-100 23483203-0 2013 Epigallocatechin gallate promotes p53 accumulation and activity via the inhibition of MDM2-mediated p53 ubiquitination in human lung cancer cells. epigallocatechin gallate 0-24 tumor protein p53 Homo sapiens 100-103 23483203-2 2013 Several studies have shown that p53 plays an important role in the activity of EGCG; however, the mechanism by which EGCG regulates p53 requires further investigation. epigallocatechin gallate 79-83 tumor protein p53 Homo sapiens 32-35 23483203-2 2013 Several studies have shown that p53 plays an important role in the activity of EGCG; however, the mechanism by which EGCG regulates p53 requires further investigation. epigallocatechin gallate 117-121 tumor protein p53 Homo sapiens 132-135 23483203-3 2013 In the present study, we showed that EGCG inhibits anchorage-independent growth of human lung cancer cells by upregulating p53 expression. epigallocatechin gallate 37-41 tumor protein p53 Homo sapiens 123-126 23483203-4 2013 EGCG treatment can substantially increase p53 stability, promote nuclear localization of p53 and decrease nuclear accumulation of MDM2. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 42-45 23483203-4 2013 EGCG treatment can substantially increase p53 stability, promote nuclear localization of p53 and decrease nuclear accumulation of MDM2. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 89-92 23483203-5 2013 We also found that EGCG increases the phosphorylation of p53 at Ser15 and Ser20 and enhances its transcriptional activity. epigallocatechin gallate 19-23 tumor protein p53 Homo sapiens 57-60 23483203-6 2013 Although EGCG promotes MDM2 expression in a p53-dependent manner, the interaction between MDM2 and p53 was significantly inhibited following EGCG treatment, which resulted in the inhibition of MDM2-mediated p53 ubiquitination. epigallocatechin gallate 9-13 tumor protein p53 Homo sapiens 44-47 23483203-6 2013 Although EGCG promotes MDM2 expression in a p53-dependent manner, the interaction between MDM2 and p53 was significantly inhibited following EGCG treatment, which resulted in the inhibition of MDM2-mediated p53 ubiquitination. epigallocatechin gallate 141-145 tumor protein p53 Homo sapiens 99-102 23483203-6 2013 Although EGCG promotes MDM2 expression in a p53-dependent manner, the interaction between MDM2 and p53 was significantly inhibited following EGCG treatment, which resulted in the inhibition of MDM2-mediated p53 ubiquitination. epigallocatechin gallate 141-145 tumor protein p53 Homo sapiens 99-102 23483203-7 2013 Thus, our results suggest that the stabilization and activation of p53 may partly contribute to the anticancer activity of EGCG. epigallocatechin gallate 123-127 tumor protein p53 Homo sapiens 67-70 23251091-0 2012 Combining the chemotherapeutic effects of epigallocatechin 3-gallate with siRNA-mediated p53 knock-down results in synergic pro-apoptotic effects. epigallocatechin gallate 42-68 tumor protein p53 Homo sapiens 89-92 22573016-9 2012 Using RT-PCR, EGCG treatment induced a significant anti-apoptotic effect in injured muscle tissues by normalizing the Bax/Bcl-2 ratio back to baseline levels and inhibiting overexpression of the p53 apoptotic gene at days 3 and 7 post-surgery. epigallocatechin gallate 14-18 tumor protein p53 Homo sapiens 195-198 22552582-3 2012 In this study, we demonstrate that green tea polyphenols (GTPs) and their major constituent, (-) epigallocatechin-3-gallate (EGCG), activate p53 through acetylation at the Lys373 and Lys382 residues by inhibiting class I HDACs in LNCaP human prostate cancer cells. epigallocatechin gallate 58-62 tumor protein p53 Homo sapiens 141-144 22552582-3 2012 In this study, we demonstrate that green tea polyphenols (GTPs) and their major constituent, (-) epigallocatechin-3-gallate (EGCG), activate p53 through acetylation at the Lys373 and Lys382 residues by inhibiting class I HDACs in LNCaP human prostate cancer cells. epigallocatechin gallate 93-123 tumor protein p53 Homo sapiens 141-144 22552582-3 2012 In this study, we demonstrate that green tea polyphenols (GTPs) and their major constituent, (-) epigallocatechin-3-gallate (EGCG), activate p53 through acetylation at the Lys373 and Lys382 residues by inhibiting class I HDACs in LNCaP human prostate cancer cells. epigallocatechin gallate 125-129 tumor protein p53 Homo sapiens 141-144 22552582-5 2012 Discontinuation of treatment with GTP/EGCG resulted in the loss of p53 acetylation at both the sites in these cells. epigallocatechin gallate 34-37 tumor protein p53 Homo sapiens 67-70 22552582-5 2012 Discontinuation of treatment with GTP/EGCG resulted in the loss of p53 acetylation at both the sites in these cells. epigallocatechin gallate 38-42 tumor protein p53 Homo sapiens 67-70 23251091-6 2012 p53siRNA promotes the convergence of the extrinsic and intrinsic pathways in a synergic manner with EGCG. epigallocatechin gallate 100-104 tumor protein p53 Homo sapiens 0-3 23808158-7 2013 Moreover, EGCG suppressed the high glucose-induced expression of c-fos, c-myc and p53. epigallocatechin gallate 10-14 tumor protein p53 Homo sapiens 82-85 23808158-8 2013 These findings suggest that EGCG protects HLEB-3 cells from high glucose-induced apoptosis by regulating the gene expression of the Bcl-2 family, c-fos, c-myc and p53. epigallocatechin gallate 28-32 tumor protein p53 Homo sapiens 163-166 22552582-7 2012 The increased GTP/EGCG-mediated p53 acetylation enhanced its binding on the promoters of p21/waf1 and Bax, which was associated with increased accumulation of cells in the G0/G1 phase of the cell cycle and induction of apoptosis. epigallocatechin gallate 14-17 tumor protein p53 Homo sapiens 32-35 22552582-7 2012 The increased GTP/EGCG-mediated p53 acetylation enhanced its binding on the promoters of p21/waf1 and Bax, which was associated with increased accumulation of cells in the G0/G1 phase of the cell cycle and induction of apoptosis. epigallocatechin gallate 18-22 tumor protein p53 Homo sapiens 32-35 22552582-8 2012 Our findings indicate that GTP/EGCG causes acetylation of p53 by inhibiting class I HDACs, a function that is likely to be part of the mechanisms that control the physiological activity of p53. epigallocatechin gallate 27-30 tumor protein p53 Homo sapiens 58-61 22552582-8 2012 Our findings indicate that GTP/EGCG causes acetylation of p53 by inhibiting class I HDACs, a function that is likely to be part of the mechanisms that control the physiological activity of p53. epigallocatechin gallate 27-30 tumor protein p53 Homo sapiens 189-192 22552582-8 2012 Our findings indicate that GTP/EGCG causes acetylation of p53 by inhibiting class I HDACs, a function that is likely to be part of the mechanisms that control the physiological activity of p53. epigallocatechin gallate 31-35 tumor protein p53 Homo sapiens 58-61 22552582-8 2012 Our findings indicate that GTP/EGCG causes acetylation of p53 by inhibiting class I HDACs, a function that is likely to be part of the mechanisms that control the physiological activity of p53. epigallocatechin gallate 31-35 tumor protein p53 Homo sapiens 189-192 19781850-5 2010 The levels of p53 were increased in the EGCG-treated cells, with a corresponding decrease in Bcl-2 and Bid protein levels as well as an increase in the Bax level. epigallocatechin gallate 40-44 tumor protein p53 Homo sapiens 14-17 23259030-0 2012 Preventive effects of epigallocatechin-3-O-gallate against replicative senescence associated with p53 acetylation in human dermal fibroblasts. epigallocatechin gallate 22-50 tumor protein p53 Homo sapiens 98-101 23259030-3 2012 The involvement of Sirt1 and acetylated p53 was examined as an underlying mechanism for the senescence preventive activity of EGCG in HDFs. epigallocatechin gallate 126-130 tumor protein p53 Homo sapiens 40-43 23259030-7 2012 Furthermore, EGCG was found to prevent serial passage- and H(2)O(2)-induced senescence in HDFs by suppressing p53 acetylation, but the Sirt1 activity was unaffected. epigallocatechin gallate 13-17 tumor protein p53 Homo sapiens 110-113 20963498-0 2011 Apoptosis of human fibrosarcoma HT-1080 cells by epigallocatechin-3-O-gallate via induction of p53 and caspases as well as suppression of Bcl-2 and phosphorylated nuclear factor-kappaB. epigallocatechin gallate 49-77 tumor protein p53 Homo sapiens 95-98 20963498-6 2011 Immunoblot analysis revealed that the expression of p53, caspase-7 and -9 as well as the ratio of Bax/Bcl-2 protein increased significantly with higher EGCG concentrations and longer incubation times. epigallocatechin gallate 152-156 tumor protein p53 Homo sapiens 52-55 20963498-10 2011 Taken together, our data indicate that HT-1080 apoptosis may be mediated through the induction of p53 and caspases by the pro-oxidant activity of internalized EGCG, as well as suppression of Bcl-2 and phosphorylated NF-kappaB by the antioxidant activity of EGCG. epigallocatechin gallate 159-163 tumor protein p53 Homo sapiens 98-101 20444544-0 2010 p53-Dependent p21-mediated growth arrest pre-empts and protects HCT116 cells from PUMA-mediated apoptosis induced by EGCG. epigallocatechin gallate 117-121 tumor protein p53 Homo sapiens 0-3 20444544-1 2010 The tumor suppressor protein p53 plays a key role in regulation of negative cellular growth in response to EGCG. epigallocatechin gallate 107-111 tumor protein p53 Homo sapiens 29-32 20444544-3 2010 Cells expressing p53 and p21 accumulate in G1 upon treatment with EGCG. epigallocatechin gallate 66-70 tumor protein p53 Homo sapiens 17-20 20444544-5 2010 Treatment with EGCG leads to induction of p53, p21 and PUMA in p21 wild-type, and p53 and PUMA in p21(-/-) cells. epigallocatechin gallate 15-19 tumor protein p53 Homo sapiens 42-45 20444544-5 2010 Treatment with EGCG leads to induction of p53, p21 and PUMA in p21 wild-type, and p53 and PUMA in p21(-/-) cells. epigallocatechin gallate 15-19 tumor protein p53 Homo sapiens 82-85 20444544-6 2010 Ablation of p53 by RNAi protects p21(-/-) cells, thus indicating a p53-dependent apoptosis by EGCG. epigallocatechin gallate 94-98 tumor protein p53 Homo sapiens 12-15 20444544-6 2010 Ablation of p53 by RNAi protects p21(-/-) cells, thus indicating a p53-dependent apoptosis by EGCG. epigallocatechin gallate 94-98 tumor protein p53 Homo sapiens 67-70 20444544-7 2010 Furthermore, analysis of cells lacking PUMA or Bax with or without p21 but with p53 reveals that all the cells expressing p53 and p21 survived after EGCG treatment. epigallocatechin gallate 149-153 tumor protein p53 Homo sapiens 80-83 20444544-7 2010 Furthermore, analysis of cells lacking PUMA or Bax with or without p21 but with p53 reveals that all the cells expressing p53 and p21 survived after EGCG treatment. epigallocatechin gallate 149-153 tumor protein p53 Homo sapiens 122-125 20444544-10 2010 Furthermore, we find that p53-dependent activation of PUMA in response to EGCG directly leads to apoptosis with out requiring Bax as is the case in response to agents that induce DNA damage. epigallocatechin gallate 74-78 tumor protein p53 Homo sapiens 26-29 19662644-0 2009 EGCG inhibits protein synthesis, lipogenesis, and cell cycle progression through activation of AMPK in p53 positive and negative human hepatoma cells. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 103-106 19781850-7 2010 Taken together, these findings indicate that the p53-mediated mitochondrial pathway and the nuclear translocation of AIF and EndoG play a crucial role in EGCG-induced apoptosis of human laryngeal epidermoid carcinoma Hep2 cells, which proceeds through a caspase-independent pathway. epigallocatechin gallate 154-158 tumor protein p53 Homo sapiens 49-52 19662644-1 2009 In the previous studies, (-)-epigallocatechin-3-gallate (EGCG) has been shown to have anticarcinogenic effects via modulation in protein expression of p53. epigallocatechin gallate 25-55 tumor protein p53 Homo sapiens 151-154 19662644-1 2009 In the previous studies, (-)-epigallocatechin-3-gallate (EGCG) has been shown to have anticarcinogenic effects via modulation in protein expression of p53. epigallocatechin gallate 57-61 tumor protein p53 Homo sapiens 151-154 19662644-2 2009 Using p53 positive Hep G2 and p53 negative Hep 3B cells, we found that treatment of EGCG resulted in dose-dependent inhibition of cellular proliferation, which suggests that the interaction of EGCG with p53 may not fully explain its inhibitory effect on proliferation. epigallocatechin gallate 84-88 tumor protein p53 Homo sapiens 6-9 19662644-2 2009 Using p53 positive Hep G2 and p53 negative Hep 3B cells, we found that treatment of EGCG resulted in dose-dependent inhibition of cellular proliferation, which suggests that the interaction of EGCG with p53 may not fully explain its inhibitory effect on proliferation. epigallocatechin gallate 84-88 tumor protein p53 Homo sapiens 30-33 19662644-2 2009 Using p53 positive Hep G2 and p53 negative Hep 3B cells, we found that treatment of EGCG resulted in dose-dependent inhibition of cellular proliferation, which suggests that the interaction of EGCG with p53 may not fully explain its inhibitory effect on proliferation. epigallocatechin gallate 84-88 tumor protein p53 Homo sapiens 30-33 19662644-6 2009 Here, we showed that EGCG activated AMPK in both p53 positive and negative human hepatoma cells. epigallocatechin gallate 21-25 tumor protein p53 Homo sapiens 49-52 19662644-10 2009 In p53 positive Hep G2 cells, EGCG blocked the progression of cell cycle at G1 phase by inducing p53 expression and further up-regulating p21 expression. epigallocatechin gallate 30-34 tumor protein p53 Homo sapiens 3-6 19662644-10 2009 In p53 positive Hep G2 cells, EGCG blocked the progression of cell cycle at G1 phase by inducing p53 expression and further up-regulating p21 expression. epigallocatechin gallate 30-34 tumor protein p53 Homo sapiens 97-100 19662644-11 2009 However, EGCG inducted apoptosis in p53 negative Hep 3B cells. epigallocatechin gallate 9-13 tumor protein p53 Homo sapiens 36-39 18492823-7 2008 Moreover, oxidized LDL increased luciferase activity of p53 in endothelial cells transfected with a p53 promoter construct, the increase of which was strikingly downregulated by EGCG and hesperetin. epigallocatechin gallate 178-182 tumor protein p53 Homo sapiens 56-59 18519674-2 2008 Recent studies have revealed that EGCG triggers cancer cells undergoing apoptosis through p53-dependent pathway. epigallocatechin gallate 34-38 tumor protein p53 Homo sapiens 90-93 18519674-3 2008 How EGCG activates p53-dependent apoptosis is not fully understood. epigallocatechin gallate 4-8 tumor protein p53 Homo sapiens 19-22 18519674-4 2008 In the present study using JB6 cell as a model system, we have shown that EGCG can negatively regulate protein serine/threonine phosphatase-2A (PP-2A) to positively regulate p53-dependent apoptosis. epigallocatechin gallate 74-78 tumor protein p53 Homo sapiens 174-177 18519674-6 2008 Second, EGCG induces apoptosis of JB6 cells, which is associated with hyperphosphorylation of p53 and up-regulation of the proapoptotic gene, Bak. epigallocatechin gallate 8-12 tumor protein p53 Homo sapiens 94-97 18519674-8 2008 Knockdown of p53 and Bak expression with RNAi substantially inhibits EGCG-induced apoptosis. epigallocatechin gallate 69-73 tumor protein p53 Homo sapiens 13-16 18519674-12 2008 Finally, in the p53(-/-) H1299 and p53(+/+) H1080 cells, EGCG down-regulates PP-2A similarly but induces differential apoptosis. epigallocatechin gallate 57-61 tumor protein p53 Homo sapiens 16-19 18519674-12 2008 Finally, in the p53(-/-) H1299 and p53(+/+) H1080 cells, EGCG down-regulates PP-2A similarly but induces differential apoptosis. epigallocatechin gallate 57-61 tumor protein p53 Homo sapiens 35-38 18519674-13 2008 In summary, our results show that (a) PP-2A directly dephosphorylates p53 at Ser-15; (b) P53 directly controls Bak expression; and (c) EGCG negatively regulates PP-2A. epigallocatechin gallate 135-139 tumor protein p53 Homo sapiens 70-73 18519674-14 2008 Together, our results show that EGCG-mediated negative regulation of PP-2A is an important molecular event for the activation of p53-dependent apoptosis during its chemoprevention. epigallocatechin gallate 32-36 tumor protein p53 Homo sapiens 129-132 19406223-0 2009 Identification of epigallocatechin-3-gallate in green tea polyphenols as a potent inducer of p53-dependent apoptosis in the human lung cancer cell line A549. epigallocatechin gallate 18-44 tumor protein p53 Homo sapiens 93-96 19406223-6 2009 EGCg was a more potent inducer of p53-dependent transcription, and this induction was further supported by the induced level of p53 protein. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 34-37 19406223-6 2009 EGCg was a more potent inducer of p53-dependent transcription, and this induction was further supported by the induced level of p53 protein. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 128-131 19406223-7 2009 RNA interference (RNAi)-mediated p53 knockdown completely abolished EGCg-induced apoptosis. epigallocatechin gallate 68-72 tumor protein p53 Homo sapiens 33-36 19406223-9 2009 Taken together, these results indicate that EGCg, among several green tea polyphenols, is a potent apoptosis inducer that functions exclusively through a p53-dependent pathway in A549 cells. epigallocatechin gallate 44-48 tumor protein p53 Homo sapiens 154-157 18492823-7 2008 Moreover, oxidized LDL increased luciferase activity of p53 in endothelial cells transfected with a p53 promoter construct, the increase of which was strikingly downregulated by EGCG and hesperetin. epigallocatechin gallate 178-182 tumor protein p53 Homo sapiens 100-103 16506813-7 2006 Pretreatment with green tea polyphenol epigallocatechin-3-gallate (EGCG) effectively blocked peroxynitrite-induced glutathione depletion, p53 accumulation, and apoptosis in both normal and G6PD-deficient cells. epigallocatechin gallate 67-71 tumor protein p53 Homo sapiens 138-141 17624304-4 2007 EGCG has been demonstrated to inhibit the growth of a variety of cancer cells, induce apoptosis and regulate the expression of p53, myc, and ERK. epigallocatechin gallate 0-4 tumor protein p53 Homo sapiens 127-130