PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23918525-6 2013 RESULTS: RASFs displayed significantly higher caspase 3/7 activity upon camptothecin and FasL exposure when ADAM15 had been down-regulated by specific small interfering RNAs. Camptothecin 72-84 caspase 3 Homo sapiens 46-55 27768593-3 2017 Coupling ALOS4 to the topoisomerase I inhibitor Camptothecin (ALOS4-CPT) increases the cytotoxicity of CPT against human metastatic melanoma cells while reduces dramatically the cytotoxicity against non-cancerous cells as measured by the levels of gammaH2A.X, active caspase 3 and cell viability. Camptothecin 48-60 caspase 3 Homo sapiens 267-276 27035096-6 2016 Combination of PA with Eto/Cpt promoted disruption of the dynamics of actin filaments, leading to subsequent enhancement of apoptotic cell death via induction of caspase-3, -8, and -9, accompanied by increased phosphorylation of p38. Camptothecin 27-30 caspase 3 Homo sapiens 162-183 26220042-3 2016 In cell line studies, both intrinsic (spontaneous or camptothecin-induced) and extrinsic (FasL- or anti-Fas-induced) apoptosis created a high percent of MEACs over time in a process associated with caspase-3 activation, leading to cytoplasmic myosin cleavage and trafficking to cell membranes. Camptothecin 53-65 caspase 3 Homo sapiens 198-207 25906152-2 2015 We generated caspase-3 knockout (C3KO) and knockdown human colorectal cancer cells, and found that they are unexpectedly sensitized to DNA-damaging agents including 5-fluorouracil (5-FU), etoposide, and camptothecin. Camptothecin 203-215 caspase 3 Homo sapiens 13-22 25331234-8 2014 UDCA (10 muM) reduced the apoptotic effects of camptothecin (0 5 muM) by 61%, (P < 0 001) and counteracted the apoptotic effects of LCA and bilirubin determined by DNA fragmentation (56% and 60%, respectively, P < 0 001), cytometry and caspase-3 activity in Saos-2, with lower effects in hOB. Camptothecin 47-59 caspase 3 Homo sapiens 242-251 23313858-0 2013 Sirt1 attenuates camptothecin-induced apoptosis through caspase-3 pathway in porcine preadipocytes. Camptothecin 17-29 caspase 3 Homo sapiens 56-65 23313858-7 2013 Interestingly, silencing of Sirt1 significantly enhances sensitivity of porcine preadipocytes to camptothecin, which may be due to upregulation of p53, acetylated p53, Bax, cleaved caspase-3 and downregulation of Bcl-2. Camptothecin 97-109 caspase 3 Homo sapiens 181-190 21417227-2 2011 Initial biological studies indicate that psilostachyin C could enhance the sensitivity of the HeLa cell toward camptothecin (CPT) treatment via the activation of the caspase-3 mediated apoptosis pathway. Camptothecin 125-128 caspase 3 Homo sapiens 166-175 23349734-11 2013 The cleaved caspase-3 expression was significantly decreased (2.09 and 2.47 folds respectively for 5-Fluorouracil and Camptothecin) in H460 spheroid cultures compared to 2D culture system. Camptothecin 118-130 caspase 3 Homo sapiens 12-21 22970428-1 2012 A novel fluorescence derivatization method combined with HPLC was developed to detect the activity of caspase-3 and -8 in two cell lines (Hela cells and A549 cells) which were activated by low temperature-assisted ultraviolet irradiation (LT-UV), mitomycin C (MMC) and camptothecin during the apoptosis, respectively. Camptothecin 269-281 caspase 3 Homo sapiens 102-118 22976371-3 2012 This work therefore focuses on an exact evaluation of caspase-3 FMK inhibition dynamics in camptothecin-induced mesenchymal micromasses. Camptothecin 91-103 caspase 3 Homo sapiens 54-63 22528748-6 2012 The FRET-based CE system is composed of a homemade CE system and a laser source for detecting the dynamics of caspase-3 in various cells expressing sensors of caspase-3 that have been treated with anticancer drugs, such as cell cycle-independent drug cisplatin and specific cell cycle drugs camptothecin and etoposide, as well as their combination with tumor necrosis factor (TNF). Camptothecin 291-303 caspase 3 Homo sapiens 110-119 22528748-6 2012 The FRET-based CE system is composed of a homemade CE system and a laser source for detecting the dynamics of caspase-3 in various cells expressing sensors of caspase-3 that have been treated with anticancer drugs, such as cell cycle-independent drug cisplatin and specific cell cycle drugs camptothecin and etoposide, as well as their combination with tumor necrosis factor (TNF). Camptothecin 291-303 caspase 3 Homo sapiens 159-168 21515332-9 2011 Additive activity of proliferation inhibition and activation of caspase-3 by limonoids was observed when combined with camptothecin, demonstrating the induction of apoptosis. Camptothecin 119-131 caspase 3 Homo sapiens 64-73 20394499-3 2010 In search of cancer therapeutics that can overcome TRAIL resistance, we show here that celecoxib and camptothecin can sensitize TRAIL-resistant HCC cell lines, HepG2 and Hep3B, to TRAIL-induced apoptosis through downregulation of cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-inhibitory protein (c-FLIP) and cleavage of caspase-8 and caspase-3 in the HCC cells. Camptothecin 101-113 caspase 3 Homo sapiens 366-375 20925107-6 2010 The induction of apoptosis by camptothecine increases the fluorescence lifetime, which means effective cleavage of the FRET sensor by caspase-3. Camptothecin 30-43 caspase 3 Homo sapiens 134-143 19450997-7 2010 p21 Expression decreased basal caspase-3 expression compared with the untreated group, and reversed camptothecin-induced caspase-3 activity compared with camptothecin alone group. Camptothecin 100-112 caspase 3 Homo sapiens 121-130 19885006-5 2009 These results suggest that camptothecin may cause cell death in SiHa cells by inducing changes in mitochondrial membrane permeability, which leads to cytochrome c release and activation of caspase-3. Camptothecin 27-39 caspase 3 Homo sapiens 189-198 20213810-2 2010 METHODS: Caspase 3/7 activity was determined in primary OA and ADAM15-transfected T/C28a4 chondrocytes upon exposure to the DNA-damaging agent camptothecin or serum withdrawal. Camptothecin 143-155 caspase 3 Homo sapiens 9-18 20213810-8 2010 Apoptosis induction by camptothecin exposure also led to significantly elevated caspase 3/7 activity and reduced cell viability of the vector-transfected compared with ADAM15-transfected chondrocytes. Camptothecin 23-35 caspase 3 Homo sapiens 80-89 20213810-10 2010 XIAP, an inhibitor of activated caspase 3, was significantly up-regulated ( approximately 3-fold) at the protein and mRNA levels in ADAM15-transfected chondrocytes upon camptothecin treatment. Camptothecin 169-181 caspase 3 Homo sapiens 32-41 20213810-11 2010 Specific down-regulation of either ADAM15 or XIAP in OA chondrocytes led to significant sensitization to camptothecin-induced caspase 3/7 activity. Camptothecin 105-117 caspase 3 Homo sapiens 126-135 19885006-3 2009 Camptothecin caused apoptosis in SiHa cells by inducing mitochondrial membrane permeability changes that lead to the loss of mitochondrial membrane potential, decreased Bcl-2 levels, cytochrome c release, caspase-3 activation, formation of reactive oxygen species and depletion of GSH. Camptothecin 0-12 caspase 3 Homo sapiens 205-214 18923446-5 2009 In particular, pretreatment with LL-37 significantly decreased caspase-3 activity after CAM-treatment. Camptothecin 88-91 caspase 3 Homo sapiens 63-72 15862279-6 2005 Camptothecin treatment resulted in activation of caspase-3 with generation of the caspase-3 cleavage product, poly ADP-ribose polymerase (PARP). Camptothecin 0-12 caspase 3 Homo sapiens 49-58 18048937-10 2007 Infection of HeLa cells with GBS triggers pro-survival signalling and protects the HeLa cells from camptothecin-induced caspase-3 cleavage. Camptothecin 99-111 caspase 3 Homo sapiens 120-129 16962673-3 2006 In this report, using Hoechst reagent staining, reactive oxygen species production and caspase-3 activity measurement, we determined that both camptothecin and doxorubicin induced apoptosis in human thyroid carcinoma cells (FTC-133). Camptothecin 143-155 caspase 3 Homo sapiens 87-96 16598301-6 2006 Especially, AML1-ETO endows leukemic cells with the susceptibility to anti-Fas agonist antibody, ultraviolet light and camptothecin analog NSC606985-induced apoptosis with increased activation of caspase-3/8. Camptothecin 119-131 caspase 3 Homo sapiens 196-205 16374543-0 2006 Nuclear caspase-3 and caspase-7 activation, and poly(ADP-ribose) polymerase cleavage are early events in camptothecin-induced apoptosis. Camptothecin 105-117 caspase 3 Homo sapiens 8-17 18700866-7 2008 Camptothecin (CPT), however, triggered activation of caspase-3 without induction of caspase-12, and reduced cell proliferation. Camptothecin 0-12 caspase 3 Homo sapiens 53-62 18700866-7 2008 Camptothecin (CPT), however, triggered activation of caspase-3 without induction of caspase-12, and reduced cell proliferation. Camptothecin 14-17 caspase 3 Homo sapiens 53-62 18700866-8 2008 In addition, CPT-induced cell death was reversed by pre-treatment with z-DEVD, a caspase-3-specific inhibitor. Camptothecin 13-16 caspase 3 Homo sapiens 81-90 17462862-0 2007 NF-kappaB inhibition enhances caspase-3 degradation of Akt1 and apoptosis in response to camptothecin. Camptothecin 89-101 caspase 3 Homo sapiens 30-39 15862279-6 2005 Camptothecin treatment resulted in activation of caspase-3 with generation of the caspase-3 cleavage product, poly ADP-ribose polymerase (PARP). Camptothecin 0-12 caspase 3 Homo sapiens 82-91 12603831-5 2003 Surprisingly, activation of procaspase-3 preceded activation of the initiator procaspases 2, 8, 9 and 10 during CT-induced apoptosis of Y79 cells. Camptothecin 112-114 caspase 3 Homo sapiens 28-40 14504478-9 2003 Following treatment with TPT, CPT or MTX the peak of H2AX phosphorylation preceded caspase-3 activation and the appearance of apoptosis-associated DNA fragmentation, both selective to S-phase cells. Camptothecin 30-33 caspase 3 Homo sapiens 83-92 15660100-5 2005 We found that NO donors ((+/-)-S-nitroso-N-acetylpenicillamine, S-nitrosoglutathione, and NONOates) dose-dependently inhibited caspase-3 and -9 activity induced by STS and camptothecin. Camptothecin 172-184 caspase 3 Homo sapiens 127-143 12866025-3 2003 Caspase-3 activation as well as nuclear fragmentation, both indicative of apoptosis, were dose dependently inhibited by the NO-liberating agents sodium nitroprusside (SNP) or S-nitroso-N-acetyl-D,L-penicillamine (SNAP) when apoptosis was initiated by flavone with only minor effects on apoptosis when initiated by camptothecin. Camptothecin 314-326 caspase 3 Homo sapiens 0-9 12538580-2 2003 Exposure of human neuroblastoma SH-SY5Y cells to the DNA-damaging agent camptothecin increased p53 levels, activated caspase-3, and caused cell death. Camptothecin 72-84 caspase 3 Homo sapiens 117-126 33237422-7 2021 Our array data suggest that camptothecin treatment induced DNA double-strand breaks in Jurkat cells and activated the DNA damage pathways ATM and Chk2, which then further induced apoptosis through caspase 3 and PARP. Camptothecin 28-40 caspase 3 Homo sapiens 197-206 11720709-5 2001 Treatment of the differentiated SH-SY5Y cells with camptothecin resulted in a time and concentration dependent activation of caspase-3 with a concomitant increase in the presence of apoptotic nuclei. Camptothecin 51-63 caspase 3 Homo sapiens 125-134 10066379-1 1999 Treatment of 26L cells, a subclone obtained from U937 cells, with TNF-alpha or DNA-damaging agents such as teniposide (VM26) and camptothecin (CPT) induced morphologically and biochemically typical apoptotic changes, including the activation of procaspase-3. Camptothecin 129-141 caspase 3 Homo sapiens 245-257 10066379-1 1999 Treatment of 26L cells, a subclone obtained from U937 cells, with TNF-alpha or DNA-damaging agents such as teniposide (VM26) and camptothecin (CPT) induced morphologically and biochemically typical apoptotic changes, including the activation of procaspase-3. Camptothecin 143-146 caspase 3 Homo sapiens 245-257 9264376-8 1997 Taken together, these results suggest that in HL60 cells, both CPP32 and serine proteases are activated in camptothecin-induced apoptosis. Camptothecin 107-119 caspase 3 Homo sapiens 63-68 11925121-13 2002 An intact cytochrome c pathway was demonstrated in C33A cells leading to cleavage of caspase 3 after camptothecin treatment. Camptothecin 101-113 caspase 3 Homo sapiens 85-94 11753682-8 2001 Camptothecin increased caspase 3 activity twice as much in the IEX-HaCaT cells when compared to HaCaT cells. Camptothecin 0-12 caspase 3 Homo sapiens 23-32 10984607-4 2000 For IAP-expressing cells treated with camptothecin, survival correlated with their intrinsic anti-caspase-3 activity. Camptothecin 38-50 caspase 3 Homo sapiens 98-107 10845773-2 2000 We show here that this cleavage activity is lacking in camptothecin-treated caspase 3-deficient neurons. Camptothecin 55-67 caspase 3 Homo sapiens 76-85 10845773-3 2000 Moreover, we report that death of camptothecin-treated caspase 3-deficient neurons cultured from E16 embryos is delayed and that no significant increase in survival is observed with cotreatment with the general caspase inhibitor BAF. Camptothecin 34-46 caspase 3 Homo sapiens 55-64 10845773-4 2000 These results indicate that caspase-dependent death of camptothecin-treated cortical neurons requires caspase 3 activity. Camptothecin 55-67 caspase 3 Homo sapiens 102-111 10845773-6 2000 However, Bax-dependent cytochrome c release still occurs in camptothecin-treated caspase 3-deficient cortical neurons. Camptothecin 60-72 caspase 3 Homo sapiens 81-90 10205159-4 1999 Caspase-6 was found to co-purify with caspase-3 as part of a multiprotein activation complex from extracts of camptothecin-treated Jurkat cells. Camptothecin 110-122 caspase 3 Homo sapiens 38-47 9756937-5 1998 Anticancer drugs such as camptothecin, vinblastine, inostamycin, and adriamycin induced activation of caspase-3(-like) proteases and apoptosis. Camptothecin 25-37 caspase 3 Homo sapiens 102-117 9264376-4 1997 We found that CPP32 is activated during camptothecin-induced apoptosis, and that N-benzyloxycarbony-Val-Ala-Asp (O-methyl) -fluoromethyketone (Z-VAD-fmk), a cell permeable caspase inhibitor blocks all features of apoptosis: morphological changes, cleavage of caspase 3 (CPP32/Yama/Apopain) and poly(ADP-ribose) polymerase, lamin B degradation and DNA fragmentation. Camptothecin 40-52 caspase 3 Homo sapiens 14-19