PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19189638-0 2008 Role of caspases in 5-FU and selenium-induced growth inhibition of colorectal cancer cells. Fluorouracil 20-24 caspase 8 Homo sapiens 8-16 20132554-9 2010 Data from our study also demonstrated that treatment with 5-FU caused a significant increase in unmethylated CASP8 and in CASP8 mRNA in all 3 cancer lines. Fluorouracil 58-62 caspase 8 Homo sapiens 109-114 20132554-9 2010 Data from our study also demonstrated that treatment with 5-FU caused a significant increase in unmethylated CASP8 and in CASP8 mRNA in all 3 cancer lines. Fluorouracil 58-62 caspase 8 Homo sapiens 122-127 19928967-4 2009 The combinatory use of AE and 5-fluorouracil (5-Fu) achieved significantly more cell death in A431 and SCC25 cells than only the use of AE or 5-Fu, likely via regulation of caspase-8, -9, and -3 expressions. Fluorouracil 30-44 caspase 8 Homo sapiens 173-194 19928967-4 2009 The combinatory use of AE and 5-fluorouracil (5-Fu) achieved significantly more cell death in A431 and SCC25 cells than only the use of AE or 5-Fu, likely via regulation of caspase-8, -9, and -3 expressions. Fluorouracil 46-50 caspase 8 Homo sapiens 173-194 19097688-0 2009 Andrographolide enhances 5-fluorouracil-induced apoptosis via caspase-8-dependent mitochondrial pathway involving p53 participation in hepatocellular carcinoma (SMMC-7721) cells. Fluorouracil 25-39 caspase 8 Homo sapiens 62-71 19097688-8 2009 Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3. Fluorouracil 39-43 caspase 8 Homo sapiens 120-129 19097688-9 2009 Suppression of caspase-8 with the specific inhibitor z-IETD-fmk abrogates largely ANDRO/5-FU biological activity by preventing mitochondrial membrane potential disappearance, caspase-3,9 activation and subsequent apoptosis. Fluorouracil 88-92 caspase 8 Homo sapiens 15-24 19189638-6 2008 Conversely, RKO cells expressing wildtype p53, proteolytically activated caspase-8, -9, -7 and -3 and unmethylated caspase-8 were more responsive to 5-FU and selenous acid-induced apoptosis. Fluorouracil 149-153 caspase 8 Homo sapiens 73-97 19189638-6 2008 Conversely, RKO cells expressing wildtype p53, proteolytically activated caspase-8, -9, -7 and -3 and unmethylated caspase-8 were more responsive to 5-FU and selenous acid-induced apoptosis. Fluorouracil 149-153 caspase 8 Homo sapiens 73-82 18082672-8 2008 In addition, the combination 5-FU plus scFv23/TNF induced apoptosis and this synergistic effect was dependent on activation of caspase-8 and caspase-3. Fluorouracil 29-33 caspase 8 Homo sapiens 127-136 15608676-14 2005 Additionally, we show that Chk1 deficiency potentiates 5-FU efficacy through the preferential induction of the caspase-8 pathway and subsequent caspase-3 activation. Fluorouracil 55-59 caspase 8 Homo sapiens 111-120 17637740-2 2008 We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8. Fluorouracil 57-71 caspase 8 Homo sapiens 188-197 17637740-2 2008 We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8. Fluorouracil 73-77 caspase 8 Homo sapiens 188-197 17054996-6 2006 5-FU induced apoptosis primarily via a caspase-8-dependent pathway, and ADM and GEM via caspase-9. Fluorouracil 0-4 caspase 8 Homo sapiens 39-48 17016659-0 2006 Combination of 5-FU and IFNalpha enhances IFN signaling pathway and caspase-8 activity, resulting in marked apoptosis in hepatoma cell lines. Fluorouracil 15-19 caspase 8 Homo sapiens 68-77 17016659-7 2006 Caspase-3, -9, and especially caspase-8 activity was higher with IFN alpha plus 5-FU than IFN or 5-FU alone. Fluorouracil 80-84 caspase 8 Homo sapiens 30-39 17016659-7 2006 Caspase-3, -9, and especially caspase-8 activity was higher with IFN alpha plus 5-FU than IFN or 5-FU alone. Fluorouracil 97-101 caspase 8 Homo sapiens 30-39 17016659-10 2006 In conclusion, caspase-8 is the most important factor that controls IFN and 5-FU-induced apoptosis in hepatoma cell lines. Fluorouracil 76-80 caspase 8 Homo sapiens 15-24 16491956-0 2005 Irinotecan/5-fluorouracil combination induces alterations in mitochondrial membrane potential and caspases on colon cancer cell lines. Fluorouracil 11-25 caspase 8 Homo sapiens 98-106 16491956-5 2005 In this study, we verified whether the collapse in mitochondrial membrane and the activation of caspases is responsible for increased apoptosis observed with CPT-11/5-FU treatment. Fluorouracil 165-169 caspase 8 Homo sapiens 96-104 16491956-12 2005 In spite of the differences among the cell lines, these results indicated that the increase in apoptosis in HT-29 cells observed with CPT-11 followed by 5-FU treatment could be explained by a disruption in mitochondria membrane potential that induced caspases activation. Fluorouracil 153-157 caspase 8 Homo sapiens 251-259 12773255-0 2003 [Role of caspase-8 and caspase-3 in hepatoma cells apoptosis induced by 5-fluorouracil]. Fluorouracil 72-86 caspase 8 Homo sapiens 9-18 15585135-7 2004 Our experiments showed that 5-FU engaged the mitochondrial apoptotic pathway involving cytosolic cytochrome c release and subsequent activation of caspase-9 and caspase-3 as well as the membrane death receptor (DR)-mediated apoptotic pathway involving activation of caspase-8 with an Apo-1/CD95 (Fas)-dependent fashion. Fluorouracil 28-32 caspase 8 Homo sapiens 266-275 15105837-9 2004 Thus, a potential mechanism for TRAIL sensitisation by 5-FU is the increased effectiveness of caspase-8 recruitment to and activation at the DISC facilitated by the downregulation of cFLIP and the consequent shift in the ratio of caspase-8 to cFLIP at the DISC. Fluorouracil 55-59 caspase 8 Homo sapiens 94-103 15105837-9 2004 Thus, a potential mechanism for TRAIL sensitisation by 5-FU is the increased effectiveness of caspase-8 recruitment to and activation at the DISC facilitated by the downregulation of cFLIP and the consequent shift in the ratio of caspase-8 to cFLIP at the DISC. Fluorouracil 55-59 caspase 8 Homo sapiens 230-239 15130763-11 2004 In conclusion, the tyrosine kinase p56/Lck is essential for apoptosis induction by Doxorubicin, Paclitaxel and 5-Fluorouracil regulating early steps of the mitochondrial apoptosis signaling cascade, including alteration of mitochondrial functions and caspase-activation. Fluorouracil 111-125 caspase 8 Homo sapiens 251-258 12692863-0 2003 5-Fluorouracil efficiently enhanced apoptosis induced by adenovirus-mediated transfer of caspase-8 in DLD-1 colon cancer cells. Fluorouracil 0-14 caspase 8 Homo sapiens 89-98 12692863-9 2003 A potentiating effect of adenoviral treatment was also seen when 5-FU treatment was substituted by the overexpression of cyclin-dependent kinase inhibitors, p21(WAF1/CIP1) and p27(KIP1), suggesting that the cytostatic effect of 5-FU augmented apoptosis induced by caspase-8 gene transduction by inhibiting the dilution of gene products associated with cell division. Fluorouracil 65-69 caspase 8 Homo sapiens 264-273 14607657-0 2003 Caspase-8 in apoptosis of hepatoma cell induced by 5-fluorouracil. Fluorouracil 51-65 caspase 8 Homo sapiens 0-9 14607657-1 2003 OBJECTIVE: To explore the relationship between the changes in the activity of caspase-8 and apoptosis of HepG2 cells induced by 5-fluorouracil (5-Fu). Fluorouracil 128-142 caspase 8 Homo sapiens 78-87 14607657-1 2003 OBJECTIVE: To explore the relationship between the changes in the activity of caspase-8 and apoptosis of HepG2 cells induced by 5-fluorouracil (5-Fu). Fluorouracil 144-148 caspase 8 Homo sapiens 78-87 14607657-5 2003 RESULTS: After the HepG2 cells were treated with 10(-2) mol/L 5-Fu, the caspase-8 activity increased gradually and reached the peak level (313.9+/-6.9) at 16 hours, then fell down. Fluorouracil 62-66 caspase 8 Homo sapiens 72-81 14607657-7 2003 With the increasing concentration of 5-Fu, the caspase-8 activity was also increased; the activity in high concentration 5-Fu was significantly higher than that in low concentration 5-Fu (370.5+/-4.7 vs 313.7+/-6.9; 225.7+/-5.4 vs 183.3+/-4.8; 183.3+/-4.8 vs 124.0+/-6.2, P<0.01). Fluorouracil 37-41 caspase 8 Homo sapiens 47-56 14607657-7 2003 With the increasing concentration of 5-Fu, the caspase-8 activity was also increased; the activity in high concentration 5-Fu was significantly higher than that in low concentration 5-Fu (370.5+/-4.7 vs 313.7+/-6.9; 225.7+/-5.4 vs 183.3+/-4.8; 183.3+/-4.8 vs 124.0+/-6.2, P<0.01). Fluorouracil 121-125 caspase 8 Homo sapiens 47-56 14607657-7 2003 With the increasing concentration of 5-Fu, the caspase-8 activity was also increased; the activity in high concentration 5-Fu was significantly higher than that in low concentration 5-Fu (370.5+/-4.7 vs 313.7+/-6.9; 225.7+/-5.4 vs 183.3+/-4.8; 183.3+/-4.8 vs 124.0+/-6.2, P<0.01). Fluorouracil 121-125 caspase 8 Homo sapiens 47-56 14607657-8 2003 The caspase-8 activity was the highest at 1X10(-1) mol/L 5-Fu (370.5+/-4.7). Fluorouracil 57-61 caspase 8 Homo sapiens 4-13 14607657-9 2003 The caspase-8 activity in low concentration 5-Fu was higher than in the blank control group and inhibitor group (124.0+/-6.2 vs 68.5+/-3.4; 124.0+/-6.2 vs 41.0+/-2.1, P<0.01). Fluorouracil 44-48 caspase 8 Homo sapiens 4-13 14607657-12 2003 CONCLUSIONS: 5-Fu can induce apoptosis of HepG2 cells via caspase-8 signal transduction pathway, which can be blocked by IETD-FMK. Fluorouracil 13-17 caspase 8 Homo sapiens 58-67 14607657-13 2003 5-Fu promotes the increase of caspase-8 activity in a time- or concentration-dependent manner. Fluorouracil 0-4 caspase 8 Homo sapiens 30-39 12414664-7 2002 NSAIDs and 5-FU induced the mitochondrial release of cytochrome c as well as caspase-3 and -9 activation, and to a much lesser extent, caspase-8. Fluorouracil 11-15 caspase 8 Homo sapiens 135-144 11264006-8 2001 The expression of Fas-associated death domain-like interleukin 1-converting enzyme-inhibitory protein (FLIP), which acts as an inhibitor of an initiator caspase (caspase-8), was down-regulated by 5-FU treatment in cl-1 cells. Fluorouracil 196-200 caspase 8 Homo sapiens 162-171 10568827-0 1999 Apoptosis of colorectal adenocarcinoma induced by 5-FU and/or IFN-gamma through caspase 3 and caspase 8. Fluorouracil 50-54 caspase 8 Homo sapiens 94-103 11062731-8 2000 These findings suggested that 5-FU induced apoptosis was mediated by the activation of a caspase cascade involving caspase 1, 3 and 8. Fluorouracil 30-34 caspase 8 Homo sapiens 115-133 10891390-5 2000 In addition, the expression of TRAF-2 and cIAP-1, which are transcriptionally regulated by NF-kappaB and function as anti-apoptotic molecules through the interruption of caspase pathway, was also inhibited by 5-FU. Fluorouracil 209-213 caspase 8 Homo sapiens 170-177 10891390-6 2000 Finally, the activity of caspase-8 and caspase-3 showed a significant increase in response to 5-FU. Fluorouracil 94-98 caspase 8 Homo sapiens 25-34 10779637-0 2000 Morphological change, loss of deltapsi(m) and activation of caspases upon apoptosis of colorectal adenocarcinoma induced by 5-FU. Fluorouracil 124-128 caspase 8 Homo sapiens 60-68 10568827-2 1999 We examined the role of caspases on the apoptosis induction of 5-FU and IFN-gamma using a colorectal adenocarcinoma cell line. Fluorouracil 63-67 caspase 8 Homo sapiens 24-32 10568827-3 1999 The activities of caspase 3 and caspase 8 increased when apoptosis was induced by 5-FU and/or IFN-gamma. Fluorouracil 82-86 caspase 8 Homo sapiens 32-41 10568827-6 1999 Thus, caspase 3 and caspase 8 play crucial roles in apoptosis induced by 5-FU and/or IFN-gamma, regardless of the Fas-Fas ligand system. Fluorouracil 73-77 caspase 8 Homo sapiens 20-29 29695684-9 2018 Moreover, 5-fluorouracil plus circularly permuted tumor necrosis factor-related apoptosis-inducing ligand increased apoptosis-related protein levels such as cleaved caspase-3, caspase-8, and poly-ADP-ribose polymerase and downregulated that of the survival protein B-cell lymphoma-extra-large. Fluorouracil 10-24 caspase 8 Homo sapiens 176-185 32247004-12 2020 Besides, Andro markedly down-regulated the 5-Fu-induced protein expression of caspase8/3, Bax and the phosphorylation of p38. Fluorouracil 43-47 caspase 8 Homo sapiens 78-88 29921390-9 2018 The percentage of cell apoptosis increased, and the Western blot showed that the expression of caspase-3, caspase-8, and c-myc, respectively, in the semi-combination group, the 5-Fluorouracil group, and the combination group increased successively and that the successive increasing of c-myc was the most significant. Fluorouracil 177-191 caspase 8 Homo sapiens 106-115 27462786-2 2016 In the present study we aimed to investigate the clinical relevance of Plk3 expression and phosphorylation of caspase-8 at T273 in patients with anal squamous cell carcinoma (SSC) treated with 5-fluorouracil and mitomycin C-based chemoradiotherapy (CRT). Fluorouracil 193-207 caspase 8 Homo sapiens 110-119 25906152-6 2015 5-FU treatment led to the formation of a z-VAD-resistant pro-caspase-8/RIP1/FADD complex, which was strongly stabilized by caspase-3 KO. Fluorouracil 0-4 caspase 8 Homo sapiens 61-70 26785286-10 2016 CONCLUSION: These data reveal that 5-FU-induced cellular apoptosis in corneal epithelial cells may be mediated through caspase-8, caspase-9, and mitochondria-regulated pathways, as well as by upregulation of p21 and downregulation of Bcl-2-dependent signal transduction pathways. Fluorouracil 35-39 caspase 8 Homo sapiens 119-128 26692822-13 2015 In addition, As2O3 in combination with 5-FU treatment caused up-regulation of DR5, caspase 3, caspase 8, and caspase 9, and down-regulation of BCL-2, but had no effect of DR4. Fluorouracil 39-43 caspase 8 Homo sapiens 94-103 23108402-3 2013 Current knowledge states that in certain cell types, 5-FU-induced stress is signaling through a p53-dependent induction of tumor necrosis factor-receptor oligomerization required for death-inducing signaling complex formation and caspase-8 activation. Fluorouracil 53-57 caspase 8 Homo sapiens 230-239 23451189-9 2013 Curcumin potentiated 5-FU-induced expression or cleavage of pro-apoptotic proteins (caspase-8, -9, -3, PARP and Bax), and down-regulated anti-apoptotic (Bcl-xL) and proliferative (cyclin D1) proteins. Fluorouracil 21-25 caspase 8 Homo sapiens 84-101 20876774-9 2011 Mechanistic studies revealed that 5-FU-mediated suppression of c-FLIP results in increased TRAIL-induced recruitment and activation of caspase-8 at the death-inducing signalling complex (DISC), leading to caspase-3 activation and caspase-dependent cell death. Fluorouracil 34-38 caspase 8 Homo sapiens 135-144 20876774-9 2011 Mechanistic studies revealed that 5-FU-mediated suppression of c-FLIP results in increased TRAIL-induced recruitment and activation of caspase-8 at the death-inducing signalling complex (DISC), leading to caspase-3 activation and caspase-dependent cell death. Fluorouracil 34-38 caspase 8 Homo sapiens 135-142