PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33083332-0 2020 The Effects of Resveratrol Treatment on Bcl-2 and Bax Gene Expression in Endometriotic Compared with Non-Endometriotic Stromal Cells. Resveratrol 15-26 BCL2 apoptosis regulator Homo sapiens 40-45 33438556-10 2021 Furthermore expression level of Bax and Bcl2 mRNAs altered significantly in all samples treated with 50 (mug/ml) of naringenin, resveratrol, or simultaneously with both. Resveratrol 128-139 BCL2 apoptosis regulator Homo sapiens 40-44 32515014-14 2020 HBD-2 and BCL-2 exhibited increased expression in ProRoot MTA with RSV (p<0.05). Resveratrol 67-70 BCL2 apoptosis regulator Homo sapiens 10-15 33398363-6 2021 The protein expression levels of Bax, cytochrome c, cleaved caspase-9 and cleaved caspase-3 were upregulated, whereas Bcl-2 expression levels were downregulated in RSV-treated CRC cells compared with control cells. Resveratrol 164-167 BCL2 apoptosis regulator Homo sapiens 118-123 33747905-7 2021 When treated with RSV, the expression levels of full length PARP1, PCNA, and BCL-2 were found to be significantly reduced, and the expression level of Cleaved-PARP1 as well as Cleaved-Caspase3 increased significantly. Resveratrol 18-21 BCL2 apoptosis regulator Homo sapiens 77-82 33747905-10 2021 Furthermore, after RSV treatment, the anti-apoptotic index (PCNA, BCL-2) of MDA-MB-231 cells was found to decrease while the apoptosis index (caspase3) increased. Resveratrol 19-22 BCL2 apoptosis regulator Homo sapiens 66-71 32945383-8 2020 In validation experiments, RSV significantly reduced cell viability and initiated apoptosis, with an increase in the number of apoptotic cells; it also upregulated cleaved caspase-3 expression and Bax expression, and downregulated the Bcl-2 expression levels. Resveratrol 27-30 BCL2 apoptosis regulator Homo sapiens 235-240 33083332-1 2020 Background: We aimed to examine resveratrol effects on gene expression of Bcl-2, Bax and Bcl-2/Bax ratio in endometrial stromal cells derived from women with and without endometriosis. Resveratrol 32-43 BCL2 apoptosis regulator Homo sapiens 74-79 33083332-1 2020 Background: We aimed to examine resveratrol effects on gene expression of Bcl-2, Bax and Bcl-2/Bax ratio in endometrial stromal cells derived from women with and without endometriosis. Resveratrol 32-43 BCL2 apoptosis regulator Homo sapiens 89-94 33083332-4 2020 Results: Resveratrol treatment increased Bcl-2 expression in CESCs at 24 and 48 h and in EuESCs at 48 h (P<0.05), but had no significant effects on the expression of this gene in EESCs. Resveratrol 9-20 BCL2 apoptosis regulator Homo sapiens 41-46 33083332-6 2020 Regarding the Bcl-2/Bax gene expression ratio, resveratrol treatment increased Bcl-2/Bax gene expression ratio in CESCs and EuESCs at 48 h (P<0.01). Resveratrol 47-58 BCL2 apoptosis regulator Homo sapiens 14-19 33083332-6 2020 Regarding the Bcl-2/Bax gene expression ratio, resveratrol treatment increased Bcl-2/Bax gene expression ratio in CESCs and EuESCs at 48 h (P<0.01). Resveratrol 47-58 BCL2 apoptosis regulator Homo sapiens 79-84 32482196-9 2020 Furthermore, addition of resveratrol led to a decrease of ROS and MDA, and an increase in the content of T-AOC and BCL2. Resveratrol 25-36 BCL2 apoptosis regulator Homo sapiens 115-119 32477148-8 2020 In addition, our experimental results demonstrated that resveratrol markedly enhanced the decreased levels of Bcl-2 and significantly reduced the increased expression of Bax and Caspase-3 in hippocampal neurons induced by glutamate exposure. Resveratrol 56-67 BCL2 apoptosis regulator Homo sapiens 110-115 31155753-7 2019 In conclusion, our results indicate that resveratrol acts as a potential inducer to enhance the chemosensitivity of breast cancer and also suggest that miR-122-5p is involved in the pathway of cell-cycle arrest by targeting Bcl-2 and CDKs. Resveratrol 41-52 BCL2 apoptosis regulator Homo sapiens 224-229 31106631-6 2019 Resveratrol (RES), a sirtuin 1 agonist, inhibited PTH-induced apoptosis and restored Bcl-2 expression (p<.05). Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 85-90 31106631-6 2019 Resveratrol (RES), a sirtuin 1 agonist, inhibited PTH-induced apoptosis and restored Bcl-2 expression (p<.05). Resveratrol 13-16 BCL2 apoptosis regulator Homo sapiens 85-90 31155753-6 2019 Further miRNA modulation with miR-122-5p mimics or miR-122-5p inhibitors indicated a major effect of miR-122-5p on the regulation of key antiapoptotic proteins (B-cell lymphoma 2 [Bcl-2]) and cyclin-dependent kinases (CDK2, CDK4, and CDK6) in drug-resistant breast cancer cells in response to resveratrol. Resveratrol 293-304 BCL2 apoptosis regulator Homo sapiens 161-178 31228864-6 2019 In addition, resveratrol also prevented onset and progression of programmed cell death in porcine oocytes, which was confirmed by significant upregulation of the anti-apoptotic B-cell lymphoma 2 (BCL-2) gene and significant downregulation of the pro-apoptotic BCL2-associated X (BAX) gene. Resveratrol 13-24 BCL2 apoptosis regulator Homo sapiens 177-194 31228864-6 2019 In addition, resveratrol also prevented onset and progression of programmed cell death in porcine oocytes, which was confirmed by significant upregulation of the anti-apoptotic B-cell lymphoma 2 (BCL-2) gene and significant downregulation of the pro-apoptotic BCL2-associated X (BAX) gene. Resveratrol 13-24 BCL2 apoptosis regulator Homo sapiens 196-201 30588012-0 2018 Resveratrol induces apoptosis in human melanoma cell through negatively regulating Erk/PKM2/Bcl-2 axis. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 92-97 30387805-7 2019 Additionally, resveratrol treatment decreased the protein expression levels of cyclin D1, cyclin E2 and BCL2 apoptosis regulator, while it increased BCL2 associated X and tumor protein p53, all of which are involved in the regulation of cell cycle and apoptosis. Resveratrol 14-25 BCL2 apoptosis regulator Homo sapiens 104-128 30387805-7 2019 Additionally, resveratrol treatment decreased the protein expression levels of cyclin D1, cyclin E2 and BCL2 apoptosis regulator, while it increased BCL2 associated X and tumor protein p53, all of which are involved in the regulation of cell cycle and apoptosis. Resveratrol 14-25 BCL2 apoptosis regulator Homo sapiens 104-108 30881498-5 2019 Additionally, resveratrol enhanced the expression of tumour protein p53 (p53) and p53 target genes, including Bcl2 associated X, apoptosis regulator and Bcl2 binding component 3 that have a pivotal role in p53-dependent apoptosis. Resveratrol 14-25 BCL2 apoptosis regulator Homo sapiens 110-114 30881498-5 2019 Additionally, resveratrol enhanced the expression of tumour protein p53 (p53) and p53 target genes, including Bcl2 associated X, apoptosis regulator and Bcl2 binding component 3 that have a pivotal role in p53-dependent apoptosis. Resveratrol 14-25 BCL2 apoptosis regulator Homo sapiens 153-157 30657580-0 2019 Resveratrol protects against oxidative damage of retinal pigment epithelium cells by modulating SOD/MDA activity and activating Bcl-2 expression. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 128-133 30657580-13 2019 Resveratrol significantly enhanced Bcl-2 levels and decreased cleaved caspase 3 levels compared to that of H2O2 group (p<0.05). Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 35-40 30657580-14 2019 CONCLUSIONS: Resveratrol protected against the oxidative damage of RPE cells by modulating SOD/MDA activity and activating Bcl-2 expression. Resveratrol 13-24 BCL2 apoptosis regulator Homo sapiens 123-128 30588012-10 2018 Additionally, we found that resveratrol downregulated antiapoptotic protein Bcl-2 and activated Bax in the protein levels by promoting Bcl-2 degradation and cytochrome c release. Resveratrol 28-39 BCL2 apoptosis regulator Homo sapiens 76-81 30588012-10 2018 Additionally, we found that resveratrol downregulated antiapoptotic protein Bcl-2 and activated Bax in the protein levels by promoting Bcl-2 degradation and cytochrome c release. Resveratrol 28-39 BCL2 apoptosis regulator Homo sapiens 135-140 30588012-11 2018 Moreover, we discovered that PKM2, had a key role in cell apoptosis triggered by resveratrol through interacting with Bcl-2. Resveratrol 81-92 BCL2 apoptosis regulator Homo sapiens 118-123 30132966-3 2018 The current study was aimed to assess whether the apoptotic effect of resveratrol on T-cell acute lymphoblastic leukemia cell line, CCRF-CEM, is exerted through DNA methylation of BAX and BCL2 gene promoters. Resveratrol 70-81 BCL2 apoptosis regulator Homo sapiens 188-192 30588012-12 2018 Based on these results, we overexpressed PKM2 in melanoma cells and found that this prevented resveratrol-induced apoptosis by stabilizing the protein level of Bcl-2. Resveratrol 94-105 BCL2 apoptosis regulator Homo sapiens 160-165 30588012-13 2018 Conclusion: Taken together, our results provided a novel mechanism accounting for the apoptosis induction of resveratrol in melanoma cells and suggested that downregulating Erk/PKM2/Bcl-2 axis appears to be a new approach for the prevention or treatment of melanoma. Resveratrol 109-120 BCL2 apoptosis regulator Homo sapiens 182-187 30132966-6 2018 Based on our previous study, the resveratrol treatment can trigger apoptosis in CCRF-CEM cell line via upregulation of apoptotic BAX gene and downregulation of antiapoptotic BCL2 gene. Resveratrol 33-44 BCL2 apoptosis regulator Homo sapiens 174-178 30132966-8 2018 Unchanged status of DNA methylation of BAX and BCL2 genes may suggest that resveratrol causes the gene expression changes through a distinct mechanism which requires further studies to be understood. Resveratrol 75-86 BCL2 apoptosis regulator Homo sapiens 47-51 30132509-3 2018 In addition, cells treated with resveratrol displayed higher apoptotic rates, in association with mitochondrial depolarization, cytochrome c release from the mitochondrial compartment to the cytoplasm, apoptosis-inducing factor translocation from the mitochondrial compartment to the nucleus, and altered protein levels of Bcl-2, Bcl-xL and Bax. Resveratrol 32-43 BCL2 apoptosis regulator Homo sapiens 323-328 29928358-6 2018 Furthermore, resveratrol upregulated the expression of the pro-apoptotic B-cell lymphoma (Bcl)-2-associated X protein and downregulated the expression of the anti-apoptotic proteins Bcl-2 and Bcl-extra large in HeLa cells. Resveratrol 13-24 BCL2 apoptosis regulator Homo sapiens 182-187 29704506-9 2018 RSV promoted viability, inhibited apoptotic cell rate, increased Bcl-2 expression, decreased Bax, cleaved-Caspase-3, and cleaved-Caspase-9 expressions. Resveratrol 0-3 BCL2 apoptosis regulator Homo sapiens 65-70 29788929-8 2018 Mitochondrial membrane potential and apoptosis-related markers, such as an increased Bax/Bcl-2 ratio, and cleaved forms of caspase-8 and caspase-3, arise following resveratrol addition. Resveratrol 164-175 BCL2 apoptosis regulator Homo sapiens 89-94 29604279-7 2018 Resveratrol inhibited UVB-induced apoptosis by upregulating the expression of HSP27, reducing the production of proapoptotic proteins such as p65, Bax, and cleaved caspase-3, and promoting the expression of anti-apoptotic protein Bcl-2. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 230-235 29604279-8 2018 However, UVB irradiation on HaCaT cells pretreated with resveratrol led to the upregulation of Bax, downregulation of Bcl-2, and promotion of p65 and caspase-3 activation after silencing of HSP27 gene. Resveratrol 56-67 BCL2 apoptosis regulator Homo sapiens 118-123 29604279-10 2018 In summary, resveratrol plays a role in photoprotection by upregulating HSP27 expression, increasing Bcl-2/Bax ratio, and inhibiting caspase-3 activity and p65 expression. Resveratrol 12-23 BCL2 apoptosis regulator Homo sapiens 101-106 28983625-4 2017 TUNEL assay revealed that resveratrol induced cell apoptosis by increasing HCC apoptosis rate from 3+-0.78% to 16+-1.12% with upregulation of B-cell lymphoma (Bcl)-2 associated X, apoptosis regulator and cleaved-poly (ADP-Ribose) polymerase 1 (PARP), and downregulation of Bcl-2, caspase-3, caspase-7 and PARP. Resveratrol 26-37 BCL2 apoptosis regulator Homo sapiens 273-278 29662863-4 2018 Methods: In this study, we investigated the effect of different doses of resveratrol (15, 50 and 100 microM) and prednisolone (700 microM) on BAX (apoptosis promoter) and BCL2 (apoptosis inhibitor) expressions following 24 and 48 hours of treatment on CCRF-CEM cells, using real-time PCR, and on apoptosis induction using flow cytometry. Resveratrol 73-84 BCL2 apoptosis regulator Homo sapiens 171-175 29662863-7 2018 Combined resveratrol and prednisolone treatment showed synergistic effects on the overexpression of BAX and the downregulation of BCL2. Resveratrol 9-20 BCL2 apoptosis regulator Homo sapiens 130-134 29115429-7 2018 In addition, the expression of the anti-apoptosis gene B-cell lymphoma 2 (Bcl-2) was downregulated by resveratrol, and the expression of pro-apoptosis gene Bcl-2-associated X was upregulated at the mRNA and protein levels. Resveratrol 102-113 BCL2 apoptosis regulator Homo sapiens 55-72 29115429-7 2018 In addition, the expression of the anti-apoptosis gene B-cell lymphoma 2 (Bcl-2) was downregulated by resveratrol, and the expression of pro-apoptosis gene Bcl-2-associated X was upregulated at the mRNA and protein levels. Resveratrol 102-113 BCL2 apoptosis regulator Homo sapiens 74-79 29115429-7 2018 In addition, the expression of the anti-apoptosis gene B-cell lymphoma 2 (Bcl-2) was downregulated by resveratrol, and the expression of pro-apoptosis gene Bcl-2-associated X was upregulated at the mRNA and protein levels. Resveratrol 102-113 BCL2 apoptosis regulator Homo sapiens 156-161 29456707-12 2018 The present results demonstrated that Res-induced apoptosis of K562/ADM cells was autophagy-dependent and the released Cath D may trigger caspase-dependent cell death through the Bcl-2 family of proteins. Resveratrol 38-41 BCL2 apoptosis regulator Homo sapiens 179-184 28641627-13 2017 CONCLUSION: Resveratrol shows the effect of reversing the drug resisitance of HL-60/ADR cells in acute myeloid leukemia, possibly via promoting the apoptosis of HL-60/ADR cells and inhibiting the expression of MRP1, which may be related with the inhibition of BCL-2 expression and the promotion of BAX expression. Resveratrol 12-23 BCL2 apoptosis regulator Homo sapiens 260-265 29073244-5 2017 We found that 10 muM resveratrol improved the proliferation of porcine PSCs, increased the expression of A-beta-catenin (active beta-catenin), Pcna, C-Myc, Bcl-2 and sirtuin-1 (Sirt1), and decreased the expression of P53, Caspase3. Resveratrol 21-32 BCL2 apoptosis regulator Homo sapiens 156-161 28666466-15 2017 RSV had little effect on cell proliferation and only slightly affected the Bax/Bcl2 ratio. Resveratrol 0-3 BCL2 apoptosis regulator Homo sapiens 79-83 28366708-7 2017 Moreover, the simultaneous treatment of leukemia cells with ABT-737 and resveratrol resulted in a reduction in mitochondrial membrane potential, an increase of p53 protein level and up-regulation of the Bax/Bcl-2 ratio. Resveratrol 72-83 BCL2 apoptosis regulator Homo sapiens 207-212 27811363-6 2016 Moreover, resveratrol exerted an anti-apoptotic effect, as assessed by TUNEL staining, and altered the expression of the apoptosis-related genes Bax, Bcl-2 and caspase3. Resveratrol 10-21 BCL2 apoptosis regulator Homo sapiens 150-155 27779703-6 2016 In addition, resveratrol was observed to arrest cell cycle progression in G1/S phase by increasing the protein expression levels of p53 and p21, and concurrently reducing the protein expression levels of CDK2, cyclin A and cyclin E. Furthermore, resveratrol treatment significantly induced apoptosis in eosinophils, likely through the upregulation of Bim and Bax protein expression levels and the downregulation of Bcl-2 protein expression. Resveratrol 13-24 BCL2 apoptosis regulator Homo sapiens 415-420 27705937-7 2016 Up-regulated expressions of Bax, cleaved caspase-3 and down-regulated expression of Bcl-2 were observed in RSV+ MET group in comparison with RSV group either in vitro or in vivo. Resveratrol 107-110 BCL2 apoptosis regulator Homo sapiens 84-89 27506388-8 2016 RSV-GSE also induced mitochondrial-mediated apoptosis in colon CSCs characterized by elevated p53, Bax/Bcl-2 ratio and cleaved PARP. Resveratrol 0-3 BCL2 apoptosis regulator Homo sapiens 103-108 27489133-7 2016 Furthermore, RSV pretreatment substantially upregulated the expression of the SIRT1 gene by 6.8 fold, reduced the acetylation level of the forkhead transcription factor FOXO3a, and decreased the expression ratio of Bax/Bcl-2. Resveratrol 13-16 BCL2 apoptosis regulator Homo sapiens 219-224 26890143-4 2016 Resveratrol-mediated miRNA modulation regulates key anti-apoptotic and cell cycle proteins including Bcl-2, X-linked inhibitor of apoptosis protein and CDKs, which are critical for its activity. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 101-106 27050990-3 2016 Resveratrol exposure also induced an increase in Caspase-3 activity and a decrease in Bcl-2, which caused an increase in membrane permeability, and the opening of mitochondrial permeability transition pores and mitochondrial depolarization. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 86-91 26189302-6 2015 In addition, we showed that resveratrol could also activate caspase-3 and alter the Bax/Bcl-2 apoptotic signaling. Resveratrol 28-39 BCL2 apoptosis regulator Homo sapiens 88-93 25819224-5 2015 Resveratrol supported significantly higher cleavage and blastocyst formation rates than the control (80.3% and 38.0% vs. 71.1% and 22.4%, respectively) by downregulating Bax/Bcl-2, Caspase-3, and Bak. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 174-179 25819224-8 2015 On the basis of these results, we applied sequential treatments with resveratrol and trolox to SCNT, and blastocyst formation rates and total cell numbers were significantly increased compared with the control (17.2% and 52.1 vs. 11.8% and 36.6, respectively), with increased GSH, decreased ROS levels, upregulated proliferating cell nuclear antigen, and downregulated Bax/Bcl-2 and Caspase-3. Resveratrol 69-80 BCL2 apoptosis regulator Homo sapiens 373-378 26851786-6 2016 In the case of apoptotic molecules, the expression of Bax, Caspase 3 and Caspase 9 was increased significantly while the expression of anti-apoptotic molecule Bcl2 was decreased significantly in resveratrol groups with a dose-dependent manner. Resveratrol 195-206 BCL2 apoptosis regulator Homo sapiens 159-163 26573558-9 2016 However, treatment with resveratrol (12.5 microM) for 48 h significantly alleviated ioxitalamate (30 mg/ml)-induced cytotoxicity, by reducing cytosolic DNA fragmentation, increasing the expression of the anti-apoptotic protein, Bcl-2 (B-cell lymphoma 2), and survivin, activating caspase-3, preventing autophagic death and suppressing the production of reactive oxygen species (ROS). Resveratrol 24-35 BCL2 apoptosis regulator Homo sapiens 228-233 26573558-9 2016 However, treatment with resveratrol (12.5 microM) for 48 h significantly alleviated ioxitalamate (30 mg/ml)-induced cytotoxicity, by reducing cytosolic DNA fragmentation, increasing the expression of the anti-apoptotic protein, Bcl-2 (B-cell lymphoma 2), and survivin, activating caspase-3, preventing autophagic death and suppressing the production of reactive oxygen species (ROS). Resveratrol 24-35 BCL2 apoptosis regulator Homo sapiens 235-252 26314326-4 2015 It has been found that resveratrol inhibited the proliferation of H838 and H520 cells in a dose- and time-dependent manner, and apoptosis was increased in cells treated with resveratrol which was associated with the depolarization of mitochondrial membrane potential, release of cytochrome c from mitochondria to cytosol, and abnormal expression of Bcl-2 and Bax proteins. Resveratrol 23-34 BCL2 apoptosis regulator Homo sapiens 349-354 26314326-4 2015 It has been found that resveratrol inhibited the proliferation of H838 and H520 cells in a dose- and time-dependent manner, and apoptosis was increased in cells treated with resveratrol which was associated with the depolarization of mitochondrial membrane potential, release of cytochrome c from mitochondria to cytosol, and abnormal expression of Bcl-2 and Bax proteins. Resveratrol 174-185 BCL2 apoptosis regulator Homo sapiens 349-354 26314326-5 2015 Above all, resveratrol enhanced the effects of cisplatin on inhibition of cancer cell proliferation, induction of cell apoptosis, depolarization of mitochondrial membrane potential, release of cytochrome c and regulation on expression of Bcl-2 and Bax. Resveratrol 11-22 BCL2 apoptosis regulator Homo sapiens 238-243 25776512-11 2015 CONCLUSIONS: Taken together, the results of our study clearly suggested that the cell death induced by the combination of RSV-GNPs would involve alteration in expression of p53, p21, caspase-3, Bax, Bcl-2 and NF-kappaB, indicating oxidative mechanism in NCI-H460 cells. Resveratrol 122-125 BCL2 apoptosis regulator Homo sapiens 199-204 25776512-9 2015 Moreover, Western blotting analysis showed that apoptosis induced by RSV-GNPs is associated with the increased Bax, p53, p21, caspase-3 protein levels, and decreased Bcl-2 and NF-kappaB proteins expression, which indicates the involvement of mitochondria-dependent apoptosis in the anticancer efficacy of RSV-GNPs in NCI-H460 cells. Resveratrol 69-72 BCL2 apoptosis regulator Homo sapiens 166-171 25547582-14 2014 When resveratrol (5.0, 15.0, 25.0, 35.0 mg/L) was added to 25.0 mmol/L glucose medium, respectively, the apoptotic cells were decreased, the expression of pro-apoptotic protein Bax was decreased and anti-apoptotic protein Bcl-2 was increased.Intracellular ROS (compared with the basic concentration of 5.5 mmol/L, F values were 14.76, 7.018, 13.96, 4.733, 1.921, P values were 0.000, 0.000, 0.003, 0.086, 0.100 respectively) and MDA (compared with the basic concentration of 5.5 mmol/L, F values were 2.454, 1.108, 1.630, 1.563, 2.250, P values were 0.000, 0.001, 0.026, 0.068, 0.183 respectively) were decreased. Resveratrol 5-16 BCL2 apoptosis regulator Homo sapiens 222-227 25296980-6 2014 RES+CUR compared to CUR increased the PARP-1 cleavage, the Bax/Bcl-2 ratio, the inhibition of ERK1 and ERK2 phosphorylation, and the expression of LC3 II simultaneously with the formation of autophagic vacuoles. Resveratrol 0-4 BCL2 apoptosis regulator Homo sapiens 63-68 25269486-3 2014 Resveratrol inhibited proliferation and induced apoptosis in HepG2 cells via activation of caspase-9 and caspase-3, upregulation of the Bax/Bcl-2 ratio and induction of p53 expression. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 140-145 24761411-11 2014 In addition to survivin restoration, resveratrol cotreatment also induced restoration of Bcl-2/caspase-3 expression suppressed by oxaliplatin only treatment. Resveratrol 37-48 BCL2 apoptosis regulator Homo sapiens 89-94 24535223-0 2014 Resveratrol induces apoptosis of bladder cancer cells via miR-21 regulation of the Akt/Bcl-2 signaling pathway. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 87-92 24535223-7 2014 Resveratrol decreased the expression of miR-21, the level of phospho-Akt and Bcl-2 protein expression. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 77-82 24535223-11 2014 Collectively, data revealed that the effect of resveratrol on bladder cancer cell apoptosis was due to miR-21 regulation of the Akt/Bcl-2 signaling pathway. Resveratrol 47-58 BCL2 apoptosis regulator Homo sapiens 132-137 23522452-10 2013 The pro-apoptotic effect of XRT/RSV correlated with decreased expression of the anti-apoptotic molecule FLIP, Bcl-2, and survivin. Resveratrol 32-35 BCL2 apoptosis regulator Homo sapiens 110-115 23359184-0 2013 Resveratrol induces apoptosis of pancreatic cancers cells by inhibiting miR-21 regulation of BCL-2 expression. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 93-98 23359184-10 2013 Over-expression of miR-21 expression can reverse down-regulation of BCL-2 expression and apoptosis induced by resveratrol. Resveratrol 110-121 BCL2 apoptosis regulator Homo sapiens 68-73 23359184-11 2013 CONCLUSIONS: In this study, we demonstrated that the effect of resveratrol on apoptosis is due to inhibiting miR-21 regulation of BCL-2 expression. Resveratrol 63-74 BCL2 apoptosis regulator Homo sapiens 130-135 24331535-6 2013 Western blotting revealed that resveratrol significantly decreased the expression of antiapoptotic proteins (Mcl-1 and Bcl-2) and increased the expression of proapoptotic proteins (Bax, Bim, and Bad), and induced cleaved-caspase-3 in a time-dependent manner. Resveratrol 31-42 BCL2 apoptosis regulator Homo sapiens 119-124 23314035-7 2013 Mechanistically, resveratrol treatment downregulated the expression of Bcl-2 and hypoxia-inducible factor-1alpha (HIF-1alpha) proteins and upregulated the expression of caspase-3 protein. Resveratrol 17-28 BCL2 apoptosis regulator Homo sapiens 83-88 22878646-8 2012 Resveratrol also increased phosphorylation of cyclic AMP-response-element-binding protein and transcription of the anti-apoptotic gene Bcl-2. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 135-140 22011009-8 2011 Real time PCR revealed that expression of Bax and Bcl-2 was simultaneously elevated on combination of resveratrol with doxorubicin or docetaxel in all tested cell lines, whereas p53 exhibited marginal elevation in MCF-7 and HepG2 cells. Resveratrol 102-113 BCL2 apoptosis regulator Homo sapiens 50-55 22673012-3 2012 It has been shown that resveratrol inhibits the activation of Nf-kappaB and subsequently down regulates the expression of Nf-kappaB regulated genes such as interleukin-2 and Bcl-2, leading to cell cycle arrest and increased apoptosis in multiple myeloma cells. Resveratrol 23-34 BCL2 apoptosis regulator Homo sapiens 174-179 22386766-11 2012 Modulation of Bcl-2 protein induced by Resveratrol could be mediating this effect. Resveratrol 39-50 BCL2 apoptosis regulator Homo sapiens 14-19 21669190-3 2011 Helenalin, a sesquiterpene lactone (STL), induces cell death and abrogates clonal survival in a highly apoptosis-resistant Bcl-2 overexpressing Jurkat cell line as well as in two other Bcl-2 overexpressing solid tumor cell lines (mammary MCF-7; pancreatic L6.3pl). Resveratrol 36-39 BCL2 apoptosis regulator Homo sapiens 123-128 21743969-7 2011 Significant de-phosphorylation of Akt, increased Bax expression, decreased Bcl-2 expression and cleavage of caspase-3 were also observed in resveratrol-induced apoptosis in glioblastoma cells. Resveratrol 140-151 BCL2 apoptosis regulator Homo sapiens 75-80 21161674-2 2011 However, Bcl-2, a common target of STAT3 and NF-kappaB signaling, is distinctly up-regulated in resveratrol-treated medulloblastoma cells, indicating potential effects of NF-kappaB in Bcl-2 expression and anti-medulloblastoma efficiency of resveratrol. Resveratrol 96-107 BCL2 apoptosis regulator Homo sapiens 9-14 21161674-2 2011 However, Bcl-2, a common target of STAT3 and NF-kappaB signaling, is distinctly up-regulated in resveratrol-treated medulloblastoma cells, indicating potential effects of NF-kappaB in Bcl-2 expression and anti-medulloblastoma efficiency of resveratrol. Resveratrol 96-107 BCL2 apoptosis regulator Homo sapiens 184-189 21161674-2 2011 However, Bcl-2, a common target of STAT3 and NF-kappaB signaling, is distinctly up-regulated in resveratrol-treated medulloblastoma cells, indicating potential effects of NF-kappaB in Bcl-2 expression and anti-medulloblastoma efficiency of resveratrol. Resveratrol 240-251 BCL2 apoptosis regulator Homo sapiens 9-14 21161674-4 2011 The results revealed that resveratrol activated NF-kappaB signaling in both cell lines at the 4-h treatment point, and the treated cells sequentially exhibited Bcl-2 up-regulation, neuronal-like phenotype with synaptophisin expression, and, eventually, apoptosis. Resveratrol 26-37 BCL2 apoptosis regulator Homo sapiens 160-165 21161674-9 2011 Our in-vitro and in-vivo results thus demonstrate the dual effects of NF-kappaB signaling on medulloblastoma cells by delaying resveratrol-induced apoptosis by up-regulating Bcl-2 expression or by involvement in neuronal-like differentiation in the absence of resveratrol. Resveratrol 127-138 BCL2 apoptosis regulator Homo sapiens 174-179 21277758-4 2011 Resveratrol treatment resulted in a gradual time-dependent decrease in the expression of anti-apoptotic Bcl-2 and increase in that of Bax, annexin A1, growth arrest- and DNA damage-induced gene 45alpha (GADD45alpha), and cleaved caspase-3. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 104-109 20714724-4 2011 The results of our study revealed that resveratrol induced apoptosis in CLL cells in a tumor-specific manner but did not affect non-leukemic cells, and apoptosis was associated with a decreased BCL2/BAX ratio. Resveratrol 39-50 BCL2 apoptosis regulator Homo sapiens 194-198 21304978-9 2011 Resveratrol induces apoptosis by activating capase-3/7 and inhibiting the expression of Bcl-2 and XIAP in human CSCs. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 88-93 19466539-5 2009 We also demonstrated that resveratrol or quercetin modulates mRNA levels and protein expression of Bax, a pro-apoptotic gene, and Bcl-2, an anti-apoptotic gene. Resveratrol 26-37 BCL2 apoptosis regulator Homo sapiens 130-135 22301921-9 2011 The expression of downstream target genes of the Hedgehog pathway such as Gli1, Ptc1, CCND1 and BCL-2 were significantly decreased after 12.5 muM resveratrol treatment, which demonstrated a similar change of gene expression when Gli1 was knocked down by the RNAi technique in PANC-1 cells. Resveratrol 146-157 BCL2 apoptosis regulator Homo sapiens 96-101 22301921-10 2011 Resveratrol also downregulated the expression of Gli1, Ptc1, CCND1 and BCL-2 in Gli1-overexpressed BxPC-3 cells. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 71-76 21031621-8 2010 Simultaneously, resveratrol regulated the expression of the antiapoptotic proteins Bcl-2, Bcl-xL and XIAP and the proapoptotic protein Bax. Resveratrol 16-27 BCL2 apoptosis regulator Homo sapiens 83-88 20367277-0 2010 Bcl-2 modulates resveratrol-induced ROS production by regulating mitochondrial respiration in tumor cells. Resveratrol 16-27 BCL2 apoptosis regulator Homo sapiens 0-5 20367277-5 2010 The inhibitory effect of Bcl-2 on resveratrol-induced mitochondrial O(2)(-) production is further corroborated by the neutralization of this regulatory effect upon siRNA-mediated gene silencing of Bcl-2. Resveratrol 34-45 BCL2 apoptosis regulator Homo sapiens 25-30 20367277-5 2010 The inhibitory effect of Bcl-2 on resveratrol-induced mitochondrial O(2)(-) production is further corroborated by the neutralization of this regulatory effect upon siRNA-mediated gene silencing of Bcl-2. Resveratrol 34-45 BCL2 apoptosis regulator Homo sapiens 197-202 20367277-6 2010 These data provide evidence implicating mitochondrial metabolism in the anticancer activity of resveratrol, and underscore a novel regulatory role of Bcl-2 against exogenous oxidative stress through its ability to fine tune mitochondrial respiration, and by doing so maintaining mitochondrial O(2)(-) at a level optimal for survival. Resveratrol 95-106 BCL2 apoptosis regulator Homo sapiens 150-155 21090107-7 2010 We further proved fact that resveratrol can specifically promote the activity of sirt1; moreover, activated sirt1 modulates the activity of caspase-3 and bcl-2 family, involving in transcriptional regulation of p53 and NF-kappaB through antagonizing factor-induced acetylation. Resveratrol 28-39 BCL2 apoptosis regulator Homo sapiens 154-159 19908231-7 2010 Resveratrol inhibited the proliferation of 4 different human PaCa cell lines, synergized the apoptotic effects of gemcitabine, inhibited the constitutive activation of NF-kappaB and expression of bcl-2, bcl-xL, COX-2, cyclin D1 MMP-9 and VEGF. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 196-201 20097879-7 2010 The synergistic interaction of resveratrol and TRAIL depends on the intrinsic apoptosis pathway and caspases, since Bcl-2 overexpression and the caspase inhibitor zVAD.fmk inhibit apoptosis, whereas knockdown of SIRT1 by RNA interference has no effect. Resveratrol 31-42 BCL2 apoptosis regulator Homo sapiens 116-121 20036937-8 2010 Furthermore, resveratrol also exhibits anti-apoptotic properties via regulation of apoptotic mediators such as Bax, Bcl-2, and caspase-3. Resveratrol 13-24 BCL2 apoptosis regulator Homo sapiens 116-121 20367277-4 2010 Whereas overexpression of Bcl-2 increased mitochondrial oxygen consumption and complex IV activity, CEM/Bcl-2 cells responded to the increased mitochondrial oxidative stress induced by resveratrol by significantly reducing mitochondrial respiration, complex IV activity, and O(2)(-) production, and promoted cell survival. Resveratrol 185-196 BCL2 apoptosis regulator Homo sapiens 104-109 19800779-9 2010 On knockdown analysis, genistein, resveratrol and glycitein all reduced the Bcl-2/Bax ratio in the presence of apoptosis-inducing stimuli, and estrogen receptor (ER) alpha silencing had no effect on these reductions. Resveratrol 34-45 BCL2 apoptosis regulator Homo sapiens 76-81 19426672-0 2009 A novel resveratrol derivative, HS1793, overcomes the resistance conferred by Bcl-2 in human leukemic U937 cells. Resveratrol 8-19 BCL2 apoptosis regulator Homo sapiens 78-83 19714620-13 2009 Furthermore, in the mitochondrial fraction, SIRT1 inhibition by siRNA for SIRT1 increased the amount of Bax but reduced the amount of Bcl-2, while resveratrol reduced the amount of Bax but increased the amount of Bcl-2. Resveratrol 147-158 BCL2 apoptosis regulator Homo sapiens 213-218 19549761-7 2009 Expression of Bcl-2 and caspase-3 activation increased in B cells treated with 10 mumol/L resveratrol compared with mitogen alone (P < 0.01), and trends for dose-responsive increases in Bcl-2 expression and caspase-3 activation were observed (P-trend < 0.0001). Resveratrol 90-101 BCL2 apoptosis regulator Homo sapiens 14-19 19549761-7 2009 Expression of Bcl-2 and caspase-3 activation increased in B cells treated with 10 mumol/L resveratrol compared with mitogen alone (P < 0.01), and trends for dose-responsive increases in Bcl-2 expression and caspase-3 activation were observed (P-trend < 0.0001). Resveratrol 90-101 BCL2 apoptosis regulator Homo sapiens 189-194 19549761-11 2009 These data show that human B lymphocyte proliferation and apoptosis are modified by physiological concentrations of resveratrol and suggest that exposure of human B cells to resveratrol may increase survival by upregulating Bcl-2. Resveratrol 174-185 BCL2 apoptosis regulator Homo sapiens 224-229 19441815-7 2009 The A549 and CH27 cell lines treated with resveratrol, MR-3, and HMDB showed a time-dependent reduction of mitochondrial membrane potential, and the Bax/Bcl-2 ratio increased gradually with a higher concentration of polyphenols. Resveratrol 42-53 BCL2 apoptosis regulator Homo sapiens 153-158 19885558-0 2009 A novel resveratrol analogue HS-1793 treatment overcomes the resistance conferred by Bcl-2 and is associated with the formation of mature PML nuclear bodies in renal clear cell carcinoma Caki-1 cells. Resveratrol 8-19 BCL2 apoptosis regulator Homo sapiens 85-90 19885558-3 2009 Previously we designed and synthesized the resveratrol analogue HS-1793 displaying stronger antitumor efficacy than resveratrol and further demonstrated the HS-1793 resistance conferred by Bcl-2 in human leukemic U937 cells. Resveratrol 43-54 BCL2 apoptosis regulator Homo sapiens 189-194 19885558-8 2009 Our findings show that the resveratrol analogue HS-1793 might provide a novel promising strategy for overcoming the resistance conferred by Bcl-2 via PML protein and the formation of mature PML-NBs. Resveratrol 27-38 BCL2 apoptosis regulator Homo sapiens 140-145 19631782-6 2009 Since we previously demonstrated that overexpression of Bcl-2 attenuates resveratrol-induced apoptosis in human leukemic U937 cells, resveratrol-treated U937 cells were used as a negative control. Resveratrol 73-84 BCL2 apoptosis regulator Homo sapiens 56-61 19207580-6 2009 Subsequent addition of 15 microM resveratrol (LD(50) = 23.2 microM) significantly (P < 0.05) upregulated further these genes (alpha-SMA x 6.5; TGF-beta1 x 1.9; TIMP-1 x 2.2; CD95/Fas x 13.1, TNFR-1 x 2.1; Bcl-2 x 3.6; Mcl-1 x 1.9). Resveratrol 33-44 BCL2 apoptosis regulator Homo sapiens 208-213 19639794-3 2009 RESULT: After treatment with resveratrol, MTT assay showed the growth of U251 cells was inhibited in dose-dependent and time-dependent manners, apoptosis of cells advanced stage was built up, immunohistochemical staining displayed decreased the expression of Bcl-2, Bcl-XL, STAT3 and CyclinD1 and Western blot showed that resveratrol decreased the expression of Bcl-2, Bcl-XL, STAT3 and CyclinD1, and built up Bax and Caspase-3. Resveratrol 29-40 BCL2 apoptosis regulator Homo sapiens 259-264 19639794-3 2009 RESULT: After treatment with resveratrol, MTT assay showed the growth of U251 cells was inhibited in dose-dependent and time-dependent manners, apoptosis of cells advanced stage was built up, immunohistochemical staining displayed decreased the expression of Bcl-2, Bcl-XL, STAT3 and CyclinD1 and Western blot showed that resveratrol decreased the expression of Bcl-2, Bcl-XL, STAT3 and CyclinD1, and built up Bax and Caspase-3. Resveratrol 29-40 BCL2 apoptosis regulator Homo sapiens 362-367 19538862-9 2009 RT-PCR and Western blot test showed that after the treatment of colon cancer cells with resveratrol at different concentrations (25, 50, 100 and 200 micromol/L), the expression level of bcl-2 was decreased, while expression level of bax was increased. Resveratrol 88-99 BCL2 apoptosis regulator Homo sapiens 186-191 19889203-8 2009 RESULTS: Treatment with curcumin and resveratrol suppressed NF-kappaB-regulated gene products involved in inflammation (cyclooxygenase-2, matrix metalloproteinase (MMP)-3, MMP-9, vascular endothelial growth factor), inhibited apoptosis (Bcl-2, Bcl-xL, and TNF-alpha receptor-associated factor 1) and prevented activation of caspase-3. Resveratrol 37-48 BCL2 apoptosis regulator Homo sapiens 237-242 19431020-0 2009 Effect of proliferation, cell cycle, and Bcl-2s of MCF-7 cells by resveratrol. Resveratrol 66-77 BCL2 apoptosis regulator Homo sapiens 41-46 19484992-7 2009 The gene array results showed that resveratrol greatly downregulated expression levels of Bcl-2 and MDR1. Resveratrol 35-46 BCL2 apoptosis regulator Homo sapiens 90-95 19484992-8 2009 After treated with 100 micromol/L, 200 micromol/L resveratrol, the expression level of Bcl-2 and MDR1 in KBv200 cells were markedly decreased in comparison with those untreated (t were 2.98, 3.51 and 3.12, 4.56, P < 0.05). Resveratrol 50-61 BCL2 apoptosis regulator Homo sapiens 87-92 18813800-7 2008 A significant additive effect in reducing cyclin D1 and bcl-2 expression was found when gamma-tocotrienol was added with either EGCG or resveratrol. Resveratrol 136-147 BCL2 apoptosis regulator Homo sapiens 56-61 19074850-8 2008 Resveratrol has been shown to be an APE/Ref-1 inhibitor and significant decreases in AP-1/JunD, MMP-1, Bcl-2, and iNOS protein levels occurred after exposure to resveratrol. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 103-108 19074850-8 2008 Resveratrol has been shown to be an APE/Ref-1 inhibitor and significant decreases in AP-1/JunD, MMP-1, Bcl-2, and iNOS protein levels occurred after exposure to resveratrol. Resveratrol 161-172 BCL2 apoptosis regulator Homo sapiens 103-108 18804944-10 2008 The results of gene detection showed that the expression levels of MDR1 and Bcl-2 were decreased upon resveratrol treatment. Resveratrol 102-113 BCL2 apoptosis regulator Homo sapiens 76-81 18584328-0 2008 Resveratrol disrupts peroxynitrite-triggered mitochondrial apoptotic pathway: a role for Bcl-2. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 89-94 18928588-0 2008 [Relationship between apoptotic effect of Resveratrol on KG-1 cells and expression of bcl-2/bax]. Resveratrol 42-53 BCL2 apoptosis regulator Homo sapiens 86-91 18584328-6 2008 This ratio decreased when cells where pre-incubated with 10 and 50 muM resveratrol, mainly due to resveratrol ability per se to increase Bcl-2 intracellular levels without affecting Bax intracellular levels. Resveratrol 71-82 BCL2 apoptosis regulator Homo sapiens 137-142 18584328-6 2008 This ratio decreased when cells where pre-incubated with 10 and 50 muM resveratrol, mainly due to resveratrol ability per se to increase Bcl-2 intracellular levels without affecting Bax intracellular levels. Resveratrol 98-109 BCL2 apoptosis regulator Homo sapiens 137-142 18584328-7 2008 These results propose an additional mechanism whereby resveratrol may exert its cardioprotective effects and suggest a key role for Bcl-2 in the resveratrol anti-apoptotic action, especially in disrupting peroxynitrite-triggered mitochondrial pathway. Resveratrol 145-156 BCL2 apoptosis regulator Homo sapiens 132-137 18575753-6 2008 We found that RSVL-induced apoptosis correlates with sustained activation of ERK1/2 and suppression of Bcl-2 expression. Resveratrol 14-18 BCL2 apoptosis regulator Homo sapiens 103-108 18507431-3 2008 We show that resveratrol induces apoptosis in Jeko-1 cells and modulates several key molecules, including cyclin D1 (CCND1), p53 (TP53), p21 (CDKN1A), BCL2, BAX, Bcl XL (BCL2L1), caspase 9 (CASP9) and p27 (CDKN1B). Resveratrol 13-24 BCL2 apoptosis regulator Homo sapiens 151-155 18575753-7 2008 Inhibition of ERK1/2 activation by its specific inhibitor or small interfering RNA reverses the effect of RSVL on Bcl-2 suppression and inhibits apoptosis, while overexpression of MEK1, which is directly upstream of both ERK1 and ERK2, enhances apoptosis induced by RSVL. Resveratrol 106-110 BCL2 apoptosis regulator Homo sapiens 114-119 17603292-7 2007 Resveratrol pretreatment led to a decrease in cleavage of PARP, an increase in the Bcl-2 protein, and activation of caspase-3. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 83-88 18592012-4 2008 The expression of STAT3 downstream genes, survivin, cyclin D1, Cox-2, and c-Myc, was suppressed but Bcl-2 was enhanced by resveratrol. Resveratrol 122-133 BCL2 apoptosis regulator Homo sapiens 100-105 18592012-10 2008 Enhanced leukemia inhibitory factor and Bcl-2 expressions in resveratrol-treated cells might reflect a compensatory response to the loss of STAT3 function. Resveratrol 61-72 BCL2 apoptosis regulator Homo sapiens 40-45 18428028-4 2008 RSV treatment to breast cancer cells inhibited Bcl-2 and Bcl-X(L) expression and induced mitochondrial membrane depolarization. Resveratrol 0-3 BCL2 apoptosis regulator Homo sapiens 47-52 17049120-9 2006 Resveratrol down-regulated the expression of the antiapoptotic proteins Bcl-2, Bcl-x(L) and XIAP and up-regulated the expression of the proapoptotic protein Bax. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 72-77 17050787-7 2007 In LNCaP and PC-3, the apoptosis induced by resveratrol was mediated by activation of caspases 9 and 3 and a change in the ratio of bax/bcl-2. Resveratrol 44-55 BCL2 apoptosis regulator Homo sapiens 136-141 16731767-0 2006 Resveratrol-caused apoptosis of human prostate carcinoma LNCaP cells is mediated via modulation of phosphatidylinositol 3"-kinase/Akt pathway and Bcl-2 family proteins. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 146-151 16731767-7 2006 Resveratrol treatment for LNCaP cells was also found to result in a significant (a) loss of mitochondrial membrane potential, (b) inhibition in the protein level of antiapoptotic Bcl-2, and (c) increase in proapoptotic members of the Bcl-2 family, i.e., Bax, Bak, Bid, and Bad. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 179-184 16731767-7 2006 Resveratrol treatment for LNCaP cells was also found to result in a significant (a) loss of mitochondrial membrane potential, (b) inhibition in the protein level of antiapoptotic Bcl-2, and (c) increase in proapoptotic members of the Bcl-2 family, i.e., Bax, Bak, Bid, and Bad. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 234-239 16731767-8 2006 Taken together, our data suggested that resveratrol causes an inhibition of phosphatidylinositol 3"-kinase/Akt activation that, in turn, results in modulations in Bcl-2 family proteins in such a way that the apoptosis of LNCaP cells is promoted. Resveratrol 40-51 BCL2 apoptosis regulator Homo sapiens 163-168 16490592-8 2006 Resveratrol also down-regulated the expression of NF-kappaB-regulated gene products by Western blot analysis, gelatin zymography, and enzyme-linked immunosorbent assay, including interleukin-6, Bcl-2, Bcl-xL, XIAP, c-IAP, vascular endothelial growth factor (VEGF), and matrix metalloproteinase-9 (MMP-9), which modulates an array of signals controlling cellular survival and proliferation and tumor promotion. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 194-199 15688415-0 2005 Resveratrol-induced apoptosis in MCF-7 human breast cancer cells involves a caspase-independent mechanism with downregulation of Bcl-2 and NF-kappaB. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 129-134 15763656-4 2005 Interestingly, overexpression of Bcl-2 or FADD-DN did not interfere with resveratrol-mediated cell cycle arrest or survivin depletion, but blocked release of cytochrome c and Smac from mitochondria into the cytosol, enhanced caspase activation and apoptosis upon combined treatment with resveratrol and TRAIL indicating that overexpression of Bcl-2 or FADD-DN decoupled the effect of resveratrol on the cell cycle and apoptosis. Resveratrol 287-298 BCL2 apoptosis regulator Homo sapiens 33-38 15763656-4 2005 Interestingly, overexpression of Bcl-2 or FADD-DN did not interfere with resveratrol-mediated cell cycle arrest or survivin depletion, but blocked release of cytochrome c and Smac from mitochondria into the cytosol, enhanced caspase activation and apoptosis upon combined treatment with resveratrol and TRAIL indicating that overexpression of Bcl-2 or FADD-DN decoupled the effect of resveratrol on the cell cycle and apoptosis. Resveratrol 287-298 BCL2 apoptosis regulator Homo sapiens 33-38 14744787-8 2004 Consistent with resveratrol"s ability to kill cells via nonapoptotic processes, cells transfected to express high levels of the antiapoptotic proteins Bcl-x(L) and Bcl-2 are equally sensitive as control cells to resveratrol. Resveratrol 16-27 BCL2 apoptosis regulator Homo sapiens 164-169 15480430-5 2004 In resveratrol-treated cells, tumor necrosis factor (TNF), anti-CD95 antibodies and TNF-related apoptosis-inducing ligand (TRAIL) activate a caspase-dependent death pathway that escapes Bcl-2-mediated inhibition. Resveratrol 3-14 BCL2 apoptosis regulator Homo sapiens 186-191 15517885-3 2004 The growth-inhibitory effects of resveratrol are mediated through cell-cycle arrest; upregulation of p21Cip1/WAF1, p53 and Bax; down-regulation of survivin, cyclin D1, cyclin E, Bcl-2, Bcl-xL and clAPs; and activation of caspases. Resveratrol 33-44 BCL2 apoptosis regulator Homo sapiens 178-183 12510025-2 2003 trans-Resveratrol reverses phosphorylation of Bcl-2 induced by paclitaxel and concomitantly blocks Raf-1 phosphorylation, also observed after paclitaxel exposure, thus suggesting that Bcl-2 inactivation may be dependent on the activation of the Raf/Ras cascade. Resveratrol 0-17 BCL2 apoptosis regulator Homo sapiens 46-51 12510025-3 2003 trans-Resveratrol also reverses the sustained phosphorylation of JNK/SAPK, which specifically occurs after paclitaxel exposure.Overall, our observations demonstrate that (a) the toxic action of paclitaxel on neuronal-like cells is not only related to the effect of the drug on tubulin, but also to its capacity to activate several intracellular pathways leading to inactivation of Bcl-2, thus causing cells to die by apoptosis, (b) trans-resveratrol significantly reduces paclitaxel-induced apoptosis by modulating the cellular signaling pathways which commit the cell to apoptosis. Resveratrol 0-17 BCL2 apoptosis regulator Homo sapiens 381-386 12510025-2 2003 trans-Resveratrol reverses phosphorylation of Bcl-2 induced by paclitaxel and concomitantly blocks Raf-1 phosphorylation, also observed after paclitaxel exposure, thus suggesting that Bcl-2 inactivation may be dependent on the activation of the Raf/Ras cascade. Resveratrol 0-17 BCL2 apoptosis regulator Homo sapiens 184-189 12060119-6 2002 In addition, Bcl-2 expression was also inhibited by resveratrol. Resveratrol 52-63 BCL2 apoptosis regulator Homo sapiens 13-18 12632486-8 2003 Immunohistochemical staining showed that after the treatment of EC-9706 cells with resveratrol (10 mmol/L) for 24 to 96 hours, the PRs of Bcl-2 proteins were apparently reduced with treated time (P<0.05) and the PRs of Bax proteins were apparently increased with treated time (P<0.05). Resveratrol 83-94 BCL2 apoptosis regulator Homo sapiens 138-143 12060119-7 2002 Thus, downregulation of the two anti-apoptotic proteins iNOS and Bcl-2 can contribute to the apoptotic effects of resveratrol in leukaemic B cells from chronic leukaemia. Resveratrol 114-125 BCL2 apoptosis regulator Homo sapiens 65-70 10402233-14 1999 Little changes in expression of PCNA, Rb, p53, and bcl-2 were observed in the five cell types treated with resveratrol, compared to untreated cells. Resveratrol 107-118 BCL2 apoptosis regulator Homo sapiens 51-56 10402233-15 1999 Noted exceptions included reduced expression of Rb protein and increased expression of p53 in 2beta and 2Tbeta cells, and increased expression of bcl-2 in 2beta cells, treated with resveratrol. Resveratrol 181-192 BCL2 apoptosis regulator Homo sapiens 146-151 11577002-0 2001 Bcl-2 overexpression attenuates resveratrol-induced apoptosis in U937 cells by inhibition of caspase-3 activity. Resveratrol 32-43 BCL2 apoptosis regulator Homo sapiens 0-5 11577002-2 2001 In the present study, we determined the effect of high intracellular levels of the anti-apoptosis protein Bcl-2 on caspase-3 activation, PLC-gamma1 degradation and cytochrome c release during resveratrol-induced apoptosis. Resveratrol 192-203 BCL2 apoptosis regulator Homo sapiens 106-111 11577002-7 2001 In contrast, resveratrol-induced caspase-3 activation and PLC-gamma1 degradation and apoptosis were significantly inhibited in U937/Bcl-2 cells. Resveratrol 13-24 BCL2 apoptosis regulator Homo sapiens 132-137 11577002-8 2001 Bcl-2 overexpressing cells exhibited less cytochrome c release and sustained expression levels of the IAP proteins during resveratrol-induced apoptosis. Resveratrol 122-133 BCL2 apoptosis regulator Homo sapiens 0-5 11577002-9 2001 In addition, these findings indicate that Bcl-2 inhibits resveratrol-induced apoptosis by a mechanism that interferes with cytochrome c release and activity of caspase-3 that is involved in the execution of apoptosis. Resveratrol 57-68 BCL2 apoptosis regulator Homo sapiens 42-47 11427503-0 2001 Resveratrol, a tumor-suppressive compound from grapes, induces apoptosis via a novel mitochondrial pathway controlled by Bcl-2. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 121-126 10403535-6 1999 Resveratrol treatment resulted in a gradual decrease in the expression of anti-apoptotic Bcl-2. Resveratrol 0-11 BCL2 apoptosis regulator Homo sapiens 89-94 26629245-5 2015 Furthermore, the up-regulation of Bax/Bcl-2 ratio, the activation of caspase-3 and increased cleaved PARP was also observed in K562 cells treated with resveratrol. Resveratrol 151-162 BCL2 apoptosis regulator Homo sapiens 38-43 34770968-0 2021 Effect of Resveratrol Treatment on Human Pancreatic Cancer Cells through Alterations of Bcl-2 Family Members. Resveratrol 10-21 BCL2 apoptosis regulator Homo sapiens 88-93 34326967-11 2021 Endothelial cell apoptosis was decreased by the reduction of pro-apoptotic factor Bax and increase of Bcl-2 following the incubation with resveratrol (P < 0.05). Resveratrol 138-149 BCL2 apoptosis regulator Homo sapiens 102-107 34296546-0 2021 Upregulation of MicroRNA-34a Sensitizes Ovarian Cancer Cells to Resveratrol by Targeting Bcl-2. Resveratrol 64-75 BCL2 apoptosis regulator Homo sapiens 89-94 34296546-13 2021 Further investigations revealed that overexpression of Bcl-2 significantly abolished the anti-tumor effects of REV on OC cells. Resveratrol 111-114 BCL2 apoptosis regulator Homo sapiens 55-60 34204834-4 2021 In FaDu cells, combined CisPt + RSV treatment induced an increase in apoptosis, which was associated with an increase in c-MYC and TP53 and a decrease in BCL-2 expression. Resveratrol 32-35 BCL2 apoptosis regulator Homo sapiens 154-159 34204834-5 2021 While CisPt + RSV treatment induced apoptosis in PE/CA-PJ49 cells by inhibition of BCL-2 associated with high levels of MDM-2 and subsequently led to inhibition of TP53 gene expression. Resveratrol 14-17 BCL2 apoptosis regulator Homo sapiens 83-88 35275845-11 2022 Additionally, P53, CASPASE 3, and BAX were down-regulated and BCL2 was up-regulated in the 3-NPA and Ex-527 groups; opposite trends were observed after resveratrol treatment. Resveratrol 152-163 BCL2 apoptosis regulator Homo sapiens 62-66