PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26359868-5 2015 As2O3 decreased myoblast growth at submicromolar concentrations (0.25-1 muM) after 72 h of treatment. Arsenic Trioxide 0-5 latexin Homo sapiens 72-75 15531921-3 2005 Using gelatin invasion assay and intravasation assay, we report the novel finding that low-dose ATO (1 muM) reduced the intrinsic migration ability of HeLa cells and significantly inhibited radiation-promoted tumor invasive potential of CaSki cells without inducing apoptotic cell death. Arsenic Trioxide 96-99 latexin Homo sapiens 103-106 29699374-7 2018 Our data indicated that ATO (1.618muM and 1muM in KG-1 and U937 cell lines respectively), THAL (80muM and60muM) and their combination inhibited proliferation and induced apoptosis in our cell lines. Arsenic Trioxide 24-27 latexin Homo sapiens 34-37 30946857-5 2019 Here we found that clinically achievable concentrations (0.1, 0.5 and 1 muM) of ATO resulted in a significant inhibition of proliferation during the whole process of cardiac differentiation of hiPSCs. Arsenic Trioxide 80-83 latexin Homo sapiens 72-75 30668372-8 2019 RESULTS: Pretreatment of SH-SY5Y cells with TQ (10 and 20 muM) for an hour and subsequent exposure to 2 muM As2O3 protected the SH-SY5Y cells against the neuro-damaging effects of the latter. Arsenic Trioxide 108-113 latexin Homo sapiens 58-61 30668372-8 2019 RESULTS: Pretreatment of SH-SY5Y cells with TQ (10 and 20 muM) for an hour and subsequent exposure to 2 muM As2O3 protected the SH-SY5Y cells against the neuro-damaging effects of the latter. Arsenic Trioxide 108-113 latexin Homo sapiens 104-107 29910624-4 2018 Materials and methods: The expression of Egr-1 was silenced using siRNA, and then HepG2 cells were treated with As2O3 (2 muM) and AZT (20 muM). Arsenic Trioxide 112-117 latexin Homo sapiens 121-124 29910624-7 2018 Results: The inhibitory rate of As2O3 (2 muM) combined with AZT (20 muM) on proliferation of HepG2 cells was significantly higher than that of As2O3 alone. Arsenic Trioxide 32-37 latexin Homo sapiens 41-44 29910624-7 2018 Results: The inhibitory rate of As2O3 (2 muM) combined with AZT (20 muM) on proliferation of HepG2 cells was significantly higher than that of As2O3 alone. Arsenic Trioxide 32-37 latexin Homo sapiens 68-71 29314450-3 2018 Pretreatment of SH-SY5Y cells with EA (10 and 20 muM) for 60 min followed by exposure to 2 muM As2 O3 protected the SH-SY5Y cells against the harmful effects of the second. Arsenic Trioxide 95-101 latexin Homo sapiens 91-94 26359868-7 2015 Low-concentration As2O3 (0.5 and 1 muM) significantly suppressed the myoblast cell proliferative activity, which was accompanied by a small proportion of bromodeoxyuridine (BrdU) incorporation and decreased proliferating cell nuclear antigen (PCNA) protein expression. Arsenic Trioxide 18-23 latexin Homo sapiens 35-38 26359868-8 2015 As2O3 (0.5 and 1 muM) increased the intracellular arsenic content but did not affect the reactive oxygen species (ROS) levels in the myoblasts. Arsenic Trioxide 0-5 latexin Homo sapiens 17-20 24944602-3 2014 THP-1 cells were treated with different concentrations of ATO (0, 1, 3 and 5 muM) for 24, 48 or 72 h, then tested for cell viability by CCK-8 kit, cell morphology by cytospin smear, cell apoptosis by flow cytometry, EVI-1 mRNA expression by reverse transcription polymerase chain reaction (RT-PCR) and protein quantity by western blot. Arsenic Trioxide 58-61 latexin Homo sapiens 77-80 25368250-4 2014 RESULTS: The 50% inhibitory concentrations (IC50 values) for As2O3 against proliferation of HL-60 and HL-60-R2 cells were 12.2 and 7.2 muM, while those for arsenate were >200 and 62.1 muM, respectively. Arsenic Trioxide 61-66 latexin Homo sapiens 135-138 25368250-4 2014 RESULTS: The 50% inhibitory concentrations (IC50 values) for As2O3 against proliferation of HL-60 and HL-60-R2 cells were 12.2 and 7.2 muM, while those for arsenate were >200 and 62.1 muM, respectively. Arsenic Trioxide 61-66 latexin Homo sapiens 187-190 25368250-6 2014 As2O3 and arsenate increased the proportion of apoptotic cells dose-dependently at a concentration range of 5-200 muM. Arsenic Trioxide 0-5 latexin Homo sapiens 114-117 21779797-4 2012 ATO inhibited HPF cell growth with an IC(50) of approximately 30-40 muM at 24 h and induced cell death accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsi(m)). Arsenic Trioxide 0-3 latexin Homo sapiens 68-71 21515355-4 2011 The combination of ATO (1 muM) with SS or SF at concentrations over 50 muM induced considerable cytotoxicity in all cell lines. Arsenic Trioxide 19-22 latexin Homo sapiens 26-29 21515355-4 2011 The combination of ATO (1 muM) with SS or SF at concentrations over 50 muM induced considerable cytotoxicity in all cell lines. Arsenic Trioxide 19-22 latexin Homo sapiens 71-74 21515355-6 2011 Measurements of Jurkat, HL-60 and K562 cells exposed to ATO (1 muM) and sulindacs (100 muM or 200 muM for K562 cells) indicated apoptosis as the main cell death mechanism. Arsenic Trioxide 56-59 latexin Homo sapiens 63-66 21515355-6 2011 Measurements of Jurkat, HL-60 and K562 cells exposed to ATO (1 muM) and sulindacs (100 muM or 200 muM for K562 cells) indicated apoptosis as the main cell death mechanism. Arsenic Trioxide 56-59 latexin Homo sapiens 87-90 21515355-6 2011 Measurements of Jurkat, HL-60 and K562 cells exposed to ATO (1 muM) and sulindacs (100 muM or 200 muM for K562 cells) indicated apoptosis as the main cell death mechanism. Arsenic Trioxide 56-59 latexin Homo sapiens 87-90 21315065-3 2011 We found that a non-lethal concentration of arsenic trioxide (1 muM) significantly induced the expression of heme oxygenase-1 (HO-1), a response biomarker to arsenic, without stimulating measurable superoxide production. Arsenic Trioxide 44-60 latexin Homo sapiens 64-67 21315065-5 2011 In addition, low concentrations of arsenic trioxide (1 and 2.5 muM) markedly inhibited monocyte-to-macrophage differentiation and expression of macrophage markers. Arsenic Trioxide 35-51 latexin Homo sapiens 63-66