PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29435054-7 2018 Therefore, DHA may induce apoptosis in the AMoL THP-1 cell line via currently unknown underlying molecular mechanisms, including the downregulation of ERK and Akt, and the activation of caspase-3. artenimol 11-14 caspase 3 Homo sapiens 186-195 30171707-4 2018 First, we observed that DHA could specifically inhibit the proliferation, induce apoptosis, and increase cleaved caspase-3 expression in the CNE-2Z cells. artenimol 24-27 caspase 3 Homo sapiens 113-122 30171707-9 2018 Our data demonstrated that the selective antitumor activities of DHA in NPC may occur through the specific activation of the CLC-3 Cl- channel, leading to Cl- efflux, and induced AVD, then led to [Ca2+ ]i accumulation and caspase-3 activation, and finally induced apoptosis. artenimol 65-68 caspase 3 Homo sapiens 222-231 29435054-6 2018 The protein expression of phospho-Akt and phospho-extracellular signal-regulated kinase (ERK) was also decreased, and the protein expression level of cleaved caspase-3 was increased following treatment with DHA. artenimol 207-210 caspase 3 Homo sapiens 158-167 29434895-4 2018 In the present study, it was identified that dihydroartemisinin inhibited cell viability, promoted cell apoptosis, increased B-cell lymphoma-2-associated X-protein expression, increased caspase-3/9 activities, decreased poly(ADP-ribose) polymerase levels, decreased phosphorylation of extracellular-signal-regulated kinase, and increased phosphorylation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase in colon cancer cells. artenimol 45-63 caspase 3 Homo sapiens 186-197 29309768-11 2018 The mRNA levels of apoptosis-related genes BAX and CASP3 were increased, and the anti-apoptotic gene BCL2 was decreased in oocytes exposed to DHA. artenimol 142-145 caspase 3 Homo sapiens 51-56 29434974-6 2018 RT-PCR analysis of DHA-treated or -untreated U266 cells after 48 h demonstrated a significant (P<0.01) increase in caspase-3 expression. artenimol 19-22 caspase 3 Homo sapiens 118-127 29472793-4 2018 Western blot analysis showed a significant increase in the activation of caspase-3 and expression of cleaved PARP by dihydroartemisinin treatment. artenimol 117-135 caspase 3 Homo sapiens 73-82 29434974-9 2018 The addition of SP600125 to the cells incubated with DHA resulted in a significant decrease in the caspase-3 and c-Jun expression levels compared with those cells incubated with DHA alone. artenimol 53-56 caspase 3 Homo sapiens 99-108 29434974-10 2018 These findings confirm that treatment with DHA increased caspase-3 and c-Jun expression in the U266 cells through activation of the JNK signaling pathway. artenimol 43-46 caspase 3 Homo sapiens 57-66 27900057-16 2016 Overall, the combination of DHA and DOX markedly inhibited the viability of the HeLa, OVCAR-3, MCF-7, PC-3 and A549 cells, and acted on the HeLa cells through the intrinsic apoptotic pathway mediated by caspase-9 and caspase-3. artenimol 28-31 caspase 3 Homo sapiens 217-226 29128513-10 2018 DHA activated caspase 3, caspase 8, and caspase 9 and cleaved poly (ADP-ribose) polymerase (PARP). artenimol 0-3 caspase 3 Homo sapiens 14-23 29114376-9 2017 The growth inhibition effect of DHA was related to the induction of cell apoptosis, which were manifested by annexin V-FITC staining, activation of caspase-3. artenimol 32-35 caspase 3 Homo sapiens 148-157 27401020-10 2017 Synthetic inhibitors of JNK1/2 or p38 MAPK kinase activity, but not inhibitor of ERK1/2, significantly abolished the DHA-induced activation of caspase-3 and -9. artenimol 117-120 caspase 3 Homo sapiens 143-159 25018064-7 2014 Furthermore, NAC pretreatment potently prevented DHA-induced ROS generation and loss of DeltaPsim as well as apoptosis, and silencing Bax by shRNA or inhibition of one of caspase-3, -8 and -9 also significantly prevented DHA-induced apoptosis in both cell lines, indicating the key roles of ROS and Bax as well as the caspases. artenimol 49-52 caspase 3 Homo sapiens 171-191 26457547-9 2016 More interestingly, when the caspase-3 expression was silenced using an antibody, the DHA-induced growth inhibition of A431 cells was offset significantly. artenimol 86-89 caspase 3 Homo sapiens 29-38 25701954-10 2015 Moreover, the distributions of Bid on mitochondria were increased, accompanied by the activation of caspase-3 in the presence of DHA. artenimol 129-132 caspase 3 Homo sapiens 100-109 21547369-4 2012 Cultured human metastatic melanoma cells (A375, G361, LOX) were sensitive to DHA-induced apoptosis with upregulation of cellular oxidative stress, phosphatidylserine externalization, and activational cleavage of procaspase 3. artenimol 77-80 caspase 3 Homo sapiens 212-224 25985565-0 2014 Dihydroartemisinin exhibits anti-glioma stem cell activity through inhibiting p-AKT and activating caspase-3. artenimol 0-18 caspase 3 Homo sapiens 99-108 25985565-9 2014 The data showed that Cleaved Caspase-3 increased significantly in a dose-dependent manner (p < 0.05) after the GSCs sphere cells were treated with 20, 40, and 80 muM of DHA for 24 h, which correlated with significantly decreased expression levels of p-Akt (p < 0.05). artenimol 172-175 caspase 3 Homo sapiens 29-38 25985565-10 2014 These data indicate that DHA selectively inhibits proliferation and induces apoptosis of GSCs through the down-regulation of Akt phosphorylation, which is followed by Caspase-3 activation, and these findings offer a new approach for treating gliomas. artenimol 25-28 caspase 3 Homo sapiens 167-176 24519064-6 2014 We also found that DHA decreased the mitochondrial membrane potential; activated the caspase-3, caspase-8, and caspase-9; and increased the ratio of Bax/Bcl-2. artenimol 19-22 caspase 3 Homo sapiens 85-94 24519064-8 2014 Strikingly, the free radical scavenger N-acetylcysteine or the caspase-3 inhibitor Ac-DEVD-CHO significantly prevented DHA-induced apoptotic cell death. artenimol 119-122 caspase 3 Homo sapiens 63-72 23582790-4 2013 The mechanism was at least partially due to DHA induced apoptosis by upregulating the expression of Bax, downregulating Bcl-2, Bcl-xL and Procaspase-3, and increasing caspase-9 activation, induced cell cycle arrest by downregulating cyclin E, CDK2 and CDK4. artenimol 44-47 caspase 3 Homo sapiens 138-150 23536891-3 2013 Inhibition of caspase-8 or -9 significantly blocked DHA-induced decrease of cell viability and activation of caspase-3, suggesting the dominant roles of caspase-8 and -9 in DHA-induced apoptosis. artenimol 52-55 caspase 3 Homo sapiens 109-118 23536891-3 2013 Inhibition of caspase-8 or -9 significantly blocked DHA-induced decrease of cell viability and activation of caspase-3, suggesting the dominant roles of caspase-8 and -9 in DHA-induced apoptosis. artenimol 173-176 caspase 3 Homo sapiens 109-118 33689708-0 2021 Dihydroartemisinin induces pyroptosis by promoting the AIM2/caspase-3/DFNA5 axis in breast cancer cells. artenimol 0-18 caspase 3 Homo sapiens 60-69 22994042-4 2012 RESULTS: Compared with the 0 micromol/L control group, the 25, 50 and 100 micromol/L dihydroartemisinin groups showed significantly increased apoptosis of PC-3M cells ([2.92 +/- 0.45]% vs [8.85 +/- 0.74]%, [12.83 +/- 0.84]% and [18.65 +/- 1.24]%, P < 0.01), and dose-dependent increase in the activities of caspase-8 ([0.47 +/- 0.05 ] U/microg vs [1.22 +/- 0.15], [1.76 +/- 0.07] and [2.91 +/- 0.24] U/microg, P < 0.01) and caspase-3 ([0.44 +/- 0.07] U/microg vs [0.95 +/- 0.08], [1.48 +/- 0.14] and [2.92 +/- 0.45] U/microg, P < 0.01). artenimol 85-103 caspase 3 Homo sapiens 430-439 22342732-6 2012 Activation of caspase 9 and caspase 3, but not caspase 8, was detected in DHA-treated cells. artenimol 74-77 caspase 3 Homo sapiens 28-37 21234653-9 2011 Mechanistically, DHA activated caspase-3, caspase-8, and caspase-9; upregulated the expression of Bax, FAS, and cyclin D1; downregulated the expression of Bcl-2, Cdc25B, and cyclin B1; and inhibited the activity of NF-kB. artenimol 17-20 caspase 3 Homo sapiens 31-40 20709060-2 2010 However, this report demonstrates that SP600125 synergistically enhances the dihydroartemisinin (DHA)-induced human lung adenocarcinoma cell apoptosis by accelerating Bax translocation and subsequent intrinsic apoptotic pathway involving mitochondrial membrane depolarization, cytochrome c release, caspase-9 and caspase-3 activation. artenimol 77-95 caspase 3 Homo sapiens 313-322 20709060-2 2010 However, this report demonstrates that SP600125 synergistically enhances the dihydroartemisinin (DHA)-induced human lung adenocarcinoma cell apoptosis by accelerating Bax translocation and subsequent intrinsic apoptotic pathway involving mitochondrial membrane depolarization, cytochrome c release, caspase-9 and caspase-3 activation. artenimol 97-100 caspase 3 Homo sapiens 313-322 20646665-11 2010 Western blot assay indicated that dihydroartemisinin downregulated expression of nuclear P65, and combined treatment not only downregulated the expression of Cyclin D1, Bcl-xL and Bcl-2 while upregulated Bax, thus reduced the Bcl-2/Bax ratio, but also increased the caspase-3 activation, all of which increased apoptosis in both BxPC-3 and Panc-1 cells. artenimol 34-52 caspase 3 Homo sapiens 266-275 19647441-6 2009 In this study, the FES was also used to analyze the caspase-3 activation in living cells during anti-cancer drug such as taxol, Artesunate (ART) or Dihydroartemisinin (DHA) treatment. artenimol 148-166 caspase 3 Homo sapiens 52-61 19647441-6 2009 In this study, the FES was also used to analyze the caspase-3 activation in living cells during anti-cancer drug such as taxol, Artesunate (ART) or Dihydroartemisinin (DHA) treatment. artenimol 168-171 caspase 3 Homo sapiens 52-61 19647441-7 2009 Our results showed that ART or DHA induced apoptosis by a caspase-3-dependent manner, while caspase-3 was not involved in taxol-induced cell death. artenimol 31-34 caspase 3 Homo sapiens 58-67 19272183-0 2009 Dihydroartemisinin (DHA) induces caspase-3-dependent apoptosis in human lung adenocarcinoma ASTC-a-1 cells. artenimol 0-18 caspase 3 Homo sapiens 33-42 19272183-0 2009 Dihydroartemisinin (DHA) induces caspase-3-dependent apoptosis in human lung adenocarcinoma ASTC-a-1 cells. artenimol 20-23 caspase 3 Homo sapiens 33-42 18510170-6 2008 DHA-induced DNA fragmentation also induced the activation of caspase-3 and influenced the expression of Bcl-2 and Bax. artenimol 0-3 caspase 3 Homo sapiens 61-70 34430721-7 2021 Compared with NBW piglets, IUGR piglets supplemented with DHA exhibited higher apoptosis index and caspase-3 expression, and lower proliferation index and proliferating cell nuclear antigen expression in the intestine (P < 0.05). artenimol 58-61 caspase 3 Homo sapiens 99-108 34119495-0 2021 Comments on "Dihydroartemisinin induces pyroptosis by promoting the AIM2/caspase-3/DFNA5 axis in breast cancer cells." artenimol 13-31 caspase 3 Homo sapiens 73-82 34119495-1 2021 We read the article "Dihydroartemisinin induces pyroptosis by promoting the AIM2/caspase-3/DFNA5 axis in breast cancer cells" published in Chemico-Biological Interactions. artenimol 21-39 caspase 3 Homo sapiens 81-90 34119495-2 2021 Authors revealed that dihydroartemisinin induced pyroptosis through activating the AIM2/caspase-3/DFNA5 pathway in breast cancer cells. artenimol 22-40 caspase 3 Homo sapiens 88-97 34119495-4 2021 Authors suggested that dihydroartemisinin activated AIM2/caspase-3/DFNA5 axis in MCF-7 cell line. artenimol 23-41 caspase 3 Homo sapiens 57-66 34093811-6 2021 Mechanistically, we found that ART and DHA induced apoptosis of A549 cells as evidenced by decreased protein level of VDAC and increased caspase 3 cleavage. artenimol 39-42 caspase 3 Homo sapiens 137-146 20799830-2 2010 We have previously reported that DHA induced caspase-3-dependent apoptosis in human lung adenocarcinoma cells. artenimol 33-36 caspase 3 Homo sapiens 45-54 20799830-6 2010 Confocal imaging analysis in a single living cell and Western blot assay showed that DHA triggered ROS-dependent Bax translocation, mitochondrial membrane depolarization, alteration of mitochondrial morphology, cytochrome c release, caspase-9, caspase-8, and caspase-3 activation, indicating the coexistence of ROS-mediated mitochondrial and death receptor pathway. artenimol 85-88 caspase 3 Homo sapiens 259-268 19272183-7 2009 RESULTS: Our results indicated that DHA induced apoptotic cell death in a dose- and time-dependent manner, which was accompanied by mitochondrial morphology changes, the loss of DeltaPsim and the activation of caspase-3. artenimol 36-39 caspase 3 Homo sapiens 210-219 19272183-8 2009 CONCLUSION: These results show for the first time that DHA can inhibit proliferation and induce apoptosis via caspase-3-dependent mitochondrial death pathway in ASTC-a-1 cells. artenimol 55-58 caspase 3 Homo sapiens 110-119 33689708-12 2021 Mechanistically, DHA activated the expression of absent in melanoma 2 (AIM2), caspase-3 and gasdermin E (DFNA5). artenimol 17-20 caspase 3 Homo sapiens 78-87 33689708-16 2021 Moreover, the AIM2/caspase-3/DFNA5 axis was activated by DHA and then induced pyroptosis. artenimol 57-60 caspase 3 Homo sapiens 19-28 33370709-11 2021 DHA also upregulated p53, CASP3, and cleaved-CASP3 and downregulated BCL2L1, MMP9, KDR, p-KDR, STAT1 and p-STAT1 in GC cell lines. artenimol 0-3 caspase 3 Homo sapiens 45-50 33370709-0 2021 Dihydroartemisinin inhibits the tumorigenesis and invasion of gastric cancer by regulating STAT1/KDR/MMP9 and P53/BCL2L1/CASP3/7 pathways. artenimol 0-18 caspase 3 Homo sapiens 121-128 33370709-11 2021 DHA also upregulated p53, CASP3, and cleaved-CASP3 and downregulated BCL2L1, MMP9, KDR, p-KDR, STAT1 and p-STAT1 in GC cell lines. artenimol 0-3 caspase 3 Homo sapiens 26-31 33370709-7 2021 The results indicated that the common targets of DHA and GC were enriched in multiple cancer-related pathways including KDR, STAT1 and apoptosis signaling pathways, where the core genes included KDR, MMP9, STAT1, TP53, CASP3/7 and BCL2L1. artenimol 49-52 caspase 3 Homo sapiens 219-226 33370709-12 2021 In conclusion, DHA could suppress the tumorigenesis and invasion of GC by regulating STAT1/KDR/MMP9 and p53/BCL2L1/CASP3/7 pathways. artenimol 15-18 caspase 3 Homo sapiens 115-122 31680182-7 2021 Caspase-3 mRNA and cleaved caspase-3 protein levels were markedly elevated following DHA treatment either in the presence or absence of cisplatin, suggesting a role of apoptosis in DHA-induced cell death. artenimol 85-88 caspase 3 Homo sapiens 0-9 31680182-7 2021 Caspase-3 mRNA and cleaved caspase-3 protein levels were markedly elevated following DHA treatment either in the presence or absence of cisplatin, suggesting a role of apoptosis in DHA-induced cell death. artenimol 85-88 caspase 3 Homo sapiens 27-36 31680182-7 2021 Caspase-3 mRNA and cleaved caspase-3 protein levels were markedly elevated following DHA treatment either in the presence or absence of cisplatin, suggesting a role of apoptosis in DHA-induced cell death. artenimol 181-184 caspase 3 Homo sapiens 0-9 30972796-9 2019 Compared with control and DMSO groups, the expression of HSP70 protein significantly decreased, and those of Apaf-1, caspase-3 and AIF significantly increased following treatment with DHA and quercetin for 48 hr. artenimol 184-187 caspase 3 Homo sapiens 117-126 33085744-10 2020 Furthermore, caspase-3 activity was increased after treatment with different concentrations of dihydroartemisinin. artenimol 95-113 caspase 3 Homo sapiens 13-22 33085744-11 2020 Dihydroartemisinin can induce apoptosis in protoscoleces via the ER stress-caspase-3 apoptotic pathway in vitro. artenimol 0-18 caspase 3 Homo sapiens 75-84 31534470-9 2019 DHA treatment significantly upregulated the apoptotic genes CASP3, CASP8, CASP9, and TNF. artenimol 0-3 caspase 3 Homo sapiens 60-65