PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32645343-2 2020 In the present study, we aimed to use BIBR1532, an hTERT inhibitor, in combination with ATO to sensitize MCF7 and MDA-231 cells to lower concentrations of ATO. Arsenic Trioxide 155-158 telomerase reverse transcriptase Homo sapiens 51-56 32645343-7 2020 SIGNIFICANCE: The combination of ATO and BIBR1532 synergistically induced its anti-proliferative effect in breast cancer cells by targeting the two key cancer-related pathways, hTERT and NF-kappaB, and disrupting their feed-forward loop at the same time which result in the reduction of NF-kappaB transcriptional activity and subsequent down-regulation of its target genes. Arsenic Trioxide 33-36 telomerase reverse transcriptase Homo sapiens 177-182 31539632-5 2019 Our findings also showed that BKM120 augmented ATO-induced anti-proliferative effects through inducing G1 arrest and reducing the incorporation of BrdU into the synthesized DNA of drugs-treated cells, which was coupled with c-Myc-mediated suppression of hTERT expression. Arsenic Trioxide 47-50 telomerase reverse transcriptase Homo sapiens 254-259 22944098-0 2012 Cytotoxic effect of arsenic trioxide on acute promyelocytic leukemia cells through suppression of NFkbeta-dependent induction of hTERT due to down-regulation of Pin1 transcription. Arsenic Trioxide 20-36 telomerase reverse transcriptase Homo sapiens 129-134 27039805-4 2016 ATO further upregulated expression of Bax as an important proapoptotic target of NF-kappaB and also inhibited mRNA expression of survivin, c-Myc and hTERT and suppressed telomerase activity. Arsenic Trioxide 0-3 telomerase reverse transcriptase Homo sapiens 149-154 25436934-0 2015 Arsenic trioxide suppresses transcription of hTERT through down-regulation of multiple transcription factors in HL-60 leukemia cells. Arsenic Trioxide 0-16 telomerase reverse transcriptase Homo sapiens 45-50 25436934-3 2015 We previously observed that ATO treatment induced cell death in APL cell line HL-60 accompanied by inhibition of the human telomere reverse transcriptase (hTERT) activity, a critical enzyme responsible for the control of cell replication and transformation in cancer cells. Arsenic Trioxide 28-31 telomerase reverse transcriptase Homo sapiens 155-160 25415199-0 2014 Downregulation of hTERT: an important As2O3 induced mechanism of apoptosis in myelodysplastic syndrome. Arsenic Trioxide 38-43 telomerase reverse transcriptase Homo sapiens 18-23 25415199-4 2014 As2O3 also inhibited the activities of hTERT in MUTZ-1 and SKM-1 cells. Arsenic Trioxide 0-5 telomerase reverse transcriptase Homo sapiens 39-44 25415199-7 2014 Our findings suggest that As2O3 may induce apoptosis in MUTZ-1 and SKM-1 cells by two independent pathways: first, by activation of caspase-3/8 and PARP; and second, by inhibition of NF-kappaB activity, which results in downregulation of hTERT expression. Arsenic Trioxide 26-31 telomerase reverse transcriptase Homo sapiens 238-243 25415199-8 2014 We conclude that hTERT and NF-kappaB are important molecular targets in As2O3-induced apoptosis. Arsenic Trioxide 72-77 telomerase reverse transcriptase Homo sapiens 17-22 17706770-4 2008 Characterization of expression and activity of c-Myc and its target genes hTERT (human telomerase reverse transcriptase) and CAD (carbamoyltransferase-dihydroorotase) revealed marked down-regulation in response to ATRA, but not As2O3. Arsenic Trioxide 228-233 telomerase reverse transcriptase Homo sapiens 74-79 17956674-7 2007 After treating U266 cells with 2 micromol/L As2O3 at different time points, a time-dependent reduction of procaspase-3, hTERT mRNA and protein was found without any change of bcl-2 expression. Arsenic Trioxide 44-49 telomerase reverse transcriptase Homo sapiens 120-125 17956674-9 2007 These findings suggest that the reduction of hTERT plays a critical role in the apoptosis of U266 cells induced by As2O3. Arsenic Trioxide 115-120 telomerase reverse transcriptase Homo sapiens 45-50 17643074-4 2007 Telomerase activity was not inhibited, although the level of the reverse transcriptase subunit of the human telomerase gene (hTERT) mRNA expression was down regulated during the early times and then recovered to the level found in untreated controls about 48 hours after treatment with As2O3. Arsenic Trioxide 286-291 telomerase reverse transcriptase Homo sapiens 125-130 16966277-5 2006 HL-60 and K562 were treated with arsenic trioxide (As2O3) and sodium arsenite (NaAsO2) at concentrations between 0 - 10 microM for up to 48 h. The induction of apoptosis was accompanied by down-regulation of hTERT and wt1 mRNA and protein expression but up-regulation of par-4. Arsenic Trioxide 33-49 telomerase reverse transcriptase Homo sapiens 208-213 17275888-4 2007 Coincident with the inhibition of growth, As2O3 also induced apoptosis in all cell lines as measured by the time-dependent increase in M30 antibody fluorescence (binds a caspase-cleaved epitope of cytokeratin 18) detected by flow cytometry, and reduced telomerase activity by decreasing the hTERT mRNA expression. Arsenic Trioxide 42-47 telomerase reverse transcriptase Homo sapiens 291-296 16966277-5 2006 HL-60 and K562 were treated with arsenic trioxide (As2O3) and sodium arsenite (NaAsO2) at concentrations between 0 - 10 microM for up to 48 h. The induction of apoptosis was accompanied by down-regulation of hTERT and wt1 mRNA and protein expression but up-regulation of par-4. Arsenic Trioxide 51-56 telomerase reverse transcriptase Homo sapiens 208-213 16285558-1 2005 OBJECTIVE: To study the effects and its mechanisms of arsenic trioxide (As2O3) on cell growth and human telomerase reverse transcriptase (hTERT) of human tongue cancer cells (Tca8113 cell line). Arsenic Trioxide 54-70 telomerase reverse transcriptase Homo sapiens 104-136 16285558-1 2005 OBJECTIVE: To study the effects and its mechanisms of arsenic trioxide (As2O3) on cell growth and human telomerase reverse transcriptase (hTERT) of human tongue cancer cells (Tca8113 cell line). Arsenic Trioxide 72-77 telomerase reverse transcriptase Homo sapiens 104-136 16285558-9 2005 CONCLUSION: It was suggested that As2O3 could significantly inhibit the growth of Tca8113 cells by inducing causing cell apoptosis and down-regulating the expression of hTERT mRNA gene and protein which might be one of its action mechanisms. Arsenic Trioxide 34-39 telomerase reverse transcriptase Homo sapiens 169-174 15228664-2 2004 The results showed that arsenic trioxide inhibited the growth and viability of KM(3) cell and induced apoptosis; cell cycle was arrested in G(2) phase; arsenic trioxide could inhibit telomerase activity, which consisted with the downtrend of hTERT mRNA expression. Arsenic Trioxide 24-40 telomerase reverse transcriptase Homo sapiens 242-247 15228664-2 2004 The results showed that arsenic trioxide inhibited the growth and viability of KM(3) cell and induced apoptosis; cell cycle was arrested in G(2) phase; arsenic trioxide could inhibit telomerase activity, which consisted with the downtrend of hTERT mRNA expression. Arsenic Trioxide 152-168 telomerase reverse transcriptase Homo sapiens 242-247 15228664-3 2004 In conclusion, down-regulation of telomerase activity and hTERT may play an important role in the apoptosis of MM cell line KM(3) induced by arsenic trioxide. Arsenic Trioxide 141-157 telomerase reverse transcriptase Homo sapiens 58-63