PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32521895-1 2020 PURPOSE: To explore the effects of aspirin (ASP) on the proliferation and apoptosis of HepG2 hepatocellular carcinoma (HCC) cells via the Wnt/beta-catenin signaling pathway. Aspirin 35-42 catenin beta 1 Homo sapiens 142-154 32661222-0 2020 Aspirin attenuates YAP and beta-catenin expression by promoting beta-TrCP to overcome docetaxel and vinorelbine resistance in triple-negative breast cancer. Aspirin 0-7 catenin beta 1 Homo sapiens 27-39 32661222-4 2020 Interestingly, aspirin not only significantly inhibited the growth of TNBC cells, but also attenuated YAP and beta-catenin expression by upregulating the E3 ubiquitin ligase beta-TrCP to abolished docetaxel and vinorelbine resistance. Aspirin 15-22 catenin beta 1 Homo sapiens 110-122 32521895-1 2020 PURPOSE: To explore the effects of aspirin (ASP) on the proliferation and apoptosis of HepG2 hepatocellular carcinoma (HCC) cells via the Wnt/beta-catenin signaling pathway. Aspirin 44-47 catenin beta 1 Homo sapiens 142-154 32521895-8 2020 The expression levels of TCF4 and LEF1, key molecules of the Wnt/beta-catenin signaling pathway, were lowered in HCC cells treated with 4 mM ASP, and the nuclear translocation of beta-catenin was weakened. Aspirin 141-144 catenin beta 1 Homo sapiens 65-77 32521895-8 2020 The expression levels of TCF4 and LEF1, key molecules of the Wnt/beta-catenin signaling pathway, were lowered in HCC cells treated with 4 mM ASP, and the nuclear translocation of beta-catenin was weakened. Aspirin 141-144 catenin beta 1 Homo sapiens 179-191 32521895-9 2020 The beta-catenin activator exerted a negative influence on the anticancer effect of ASP. Aspirin 84-87 catenin beta 1 Homo sapiens 4-16 32521895-10 2020 CONCLUSIONS: ASP inhibits the proliferation and promotes the apoptosis of HCC cells through the Wnt/beta-catenin signaling pathway. Aspirin 13-16 catenin beta 1 Homo sapiens 100-112 29094287-0 2018 Targeting AMPK, mTOR and beta-Catenin by Combined Metformin and Aspirin Therapy in HCC: An Appraisal in Egyptian HCC Patients. Aspirin 64-71 catenin beta 1 Homo sapiens 25-37 31824307-0 2019 Wnt/beta-Catenin Pathway-Regulated Fibromodulin Expression Is Crucial for Breast Cancer Metastasis and Inhibited by Aspirin. Aspirin 116-123 catenin beta 1 Homo sapiens 4-16 31824307-4 2019 Aspirin inhibits BCCMI by attenuating Wnt/beta-catenin signaling and suppressing FMOD expression via inhibiting deacetylation of beta-catenin by histone deacetylase 6 (HDAC6) leading to beta-catenin phosphorylation and cytoplasmic degradation. Aspirin 0-7 catenin beta 1 Homo sapiens 42-54 31824307-4 2019 Aspirin inhibits BCCMI by attenuating Wnt/beta-catenin signaling and suppressing FMOD expression via inhibiting deacetylation of beta-catenin by histone deacetylase 6 (HDAC6) leading to beta-catenin phosphorylation and cytoplasmic degradation. Aspirin 0-7 catenin beta 1 Homo sapiens 129-141 31824307-4 2019 Aspirin inhibits BCCMI by attenuating Wnt/beta-catenin signaling and suppressing FMOD expression via inhibiting deacetylation of beta-catenin by histone deacetylase 6 (HDAC6) leading to beta-catenin phosphorylation and cytoplasmic degradation. Aspirin 0-7 catenin beta 1 Homo sapiens 129-141 31824307-6 2019 Our findings identify a critical role of FMOD in cancer metastasis, reveal a mechanism regulating FMOD transcription and impacting tumor metastasis, uncover action targets and mechanism for the anticancer activity of Aspirin, and expand the understanding of the Wnt/beta-catenin pathway and tumor metastasis, which are valuable for development of cancer therapeutics. Aspirin 217-224 catenin beta 1 Homo sapiens 266-278 31663307-0 2019 Aspirin inhibits proliferation and promotes apoptosis of hepatocellular carcinoma cells via wnt/beta-catenin signaling pathway. Aspirin 0-7 catenin beta 1 Homo sapiens 96-108 29922884-0 2018 Comment on "Targeting AMPK, mTOR and beta-Catenin by Combined Metformin and Aspirin Therapy in HCC: An Appraisal in Egyptian HCC Patients". Aspirin 76-83 catenin beta 1 Homo sapiens 37-49 29094287-3 2018 OBJECTIVE: The current work aimed to investigate the possibility of targeting AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), and beta-catenin proteins through combined metformin/aspirin treatment in the HepG2 cell line, and to explore such molecular targets in Egyptian HCC patients. Aspirin 206-213 catenin beta 1 Homo sapiens 157-169 29094287-8 2018 Additionally, metformin/aspirin combined treatment enhanced cell-cell membrane localization of beta-catenin expression in HepG2 cells, which might inhibit the metastatic potential of HepG2 cells. Aspirin 24-31 catenin beta 1 Homo sapiens 95-107 29094287-10 2018 CONCLUSIONS: Targeting AMPK, mTOR and beta-catenin by combined metformin/aspirin treatment could be a promising therapeutic strategy for Egyptian HCC patients, and possibly other HCC patients. Aspirin 73-80 catenin beta 1 Homo sapiens 38-50 27055402-7 2016 Consistent with LEF1 being a downstream effector of Wnt signaling, aspirin, but not I3C, downregulated protein levels of the Wnt co-receptor LDL receptor-related protein-6 and beta-catenin and upregulated the beta-catenin destruction complex component Axin. Aspirin 67-74 catenin beta 1 Homo sapiens 176-188 29552640-7 2017 Evidence also suggests that HPGD (15-PDGH) expression levels in normal colon and the germline rs6983267 polymorphism that relates to tumor CTNNB1 (beta-catenin)/WNT signaling status may predict the efficacy of aspirin for cancer chemoprevention. Aspirin 210-217 catenin beta 1 Homo sapiens 139-145 29552640-7 2017 Evidence also suggests that HPGD (15-PDGH) expression levels in normal colon and the germline rs6983267 polymorphism that relates to tumor CTNNB1 (beta-catenin)/WNT signaling status may predict the efficacy of aspirin for cancer chemoprevention. Aspirin 210-217 catenin beta 1 Homo sapiens 147-159 27055402-7 2016 Consistent with LEF1 being a downstream effector of Wnt signaling, aspirin, but not I3C, downregulated protein levels of the Wnt co-receptor LDL receptor-related protein-6 and beta-catenin and upregulated the beta-catenin destruction complex component Axin. Aspirin 67-74 catenin beta 1 Homo sapiens 209-221 26844701-12 2016 Inhibition of COX-2 with aspirin or celecoxib did not affect Caspase-3 levels but also reduced Ki-67 and beta-Catenin levels, suggesting that Caspase-3 acted via COX-2 to stimulate cell proliferation and tissue regeneration. Aspirin 25-32 catenin beta 1 Homo sapiens 105-117 25061736-5 2014 We also used aspirin as an inhibitor of the Wnt signaling pathway in the treatment of hepG2 cells transfected with the pReceiver-M29/thy-1 expression vector to make detailed observations of apoptosis in hepG2 cells as well as the differential expression of beta-catenin, cyclinD1, and thy-1. Aspirin 13-20 catenin beta 1 Homo sapiens 257-269 22893199-7 2013 COX-independent mechanisms of aspirin, such as the inhibition of NF-kB signaling and Wnt/beta-catenin signaling and the acetylation of extra-COX proteins, have been suggested to play a role in its chemopreventive effects. Aspirin 30-37 catenin beta 1 Homo sapiens 89-101 24317174-1 2013 BACKGROUND: Regular aspirin use reduces the risk for colorectal cancer (CRC), possibly through inhibition of WNT/cadherin-associated protein beta1 (CTNNB1 or beta-catenin) signaling. Aspirin 20-27 catenin beta 1 Homo sapiens 148-154 24317174-1 2013 BACKGROUND: Regular aspirin use reduces the risk for colorectal cancer (CRC), possibly through inhibition of WNT/cadherin-associated protein beta1 (CTNNB1 or beta-catenin) signaling. Aspirin 20-27 catenin beta 1 Homo sapiens 158-170 24317174-9 2013 Moreover, among individuals with protective T allele, the effect of regular aspirin use was limited to those with positive nuclear CTNNB1 expression. Aspirin 76-83 catenin beta 1 Homo sapiens 131-137 24317174-11 2013 CONCLUSIONS: Our results support an influence of aspirin on WNT/CTNNB1 signaling and suggest that aspirin chemoprevention may be tailored according to rs6983267 genotype. Aspirin 49-56 catenin beta 1 Homo sapiens 64-70 23896061-0 2013 Hydrogen sulfide-releasing aspirin inhibits the growth of leukemic Jurkat cells and modulates beta-catenin expression. Aspirin 27-34 catenin beta 1 Homo sapiens 94-106 23230963-0 2013 Aspirin-/TMZ-coloaded microspheres exert synergistic antiglioma efficacy via inhibition of beta-catenin transactivation. Aspirin 0-7 catenin beta 1 Homo sapiens 91-103 23230963-4 2013 RESULTS: Aspirin microsphere treatment induced slight apoptosis and modestly inhibited proliferation of LN229 and U87 cells in vitro and in vivo through inhibition of beta-catenin transactivation. Aspirin 9-16 catenin beta 1 Homo sapiens 167-179 23230963-9 2013 CONCLUSIONS: Aspirin sensitized TMZ chemotherapy efficacy through inhibition of beta-catenin transactivation; furthermore, the coloaded microspheres achieved a sustained release action to reduce the TMZ dosage, offering the potential for improved treatment of glioblastomas. Aspirin 13-20 catenin beta 1 Homo sapiens 80-92 19706045-10 2009 Stimulation of COX-2 expression by aspirin was further enhanced following stimulation of the Wnt/beta-catenin pathway. Aspirin 35-42 catenin beta 1 Homo sapiens 97-109 21720709-3 2011 Using aspirin, we found that the expression levels of AKT1 in glioma cells significantly correlated with the transcriptional activity of beta-catenin. Aspirin 6-13 catenin beta 1 Homo sapiens 137-149 21406194-6 2011 Using a modified biotin switch assay we demonstrated that NO-ASA S-nitrosylates the signaling proteins p53, beta-catenin, and NF-kappaB, in colon cancer cells in a time- and concentration-dependent manner. Aspirin 61-64 catenin beta 1 Homo sapiens 108-120 21205744-6 2011 In agreement with our in vivo results, both S-ibuprofen and aspirin were found to decrease total levels of beta-catenin while increasing its phosphorylation. Aspirin 60-67 catenin beta 1 Homo sapiens 107-119 24281340-5 2012 COX-independent mechanisms of aspirin, such as the inhibition of Wnt/ b-catenin and NF-kB signaling and the acetylation of extra-COX proteins, have been suggested to play a role in its chemo-preventive effects, but their relevance remains to be demonstrated in vivo at clinical doses. Aspirin 30-37 catenin beta 1 Homo sapiens 70-79 23110215-4 2012 Moreover, we also showed by RNA interference that beta-catenin, an important target of aspirin in some studies, is an Sp-regulated gene. Aspirin 87-94 catenin beta 1 Homo sapiens 50-62 21721879-4 2011 Reverse transcriptase polymerase chain reaction and Western blot analyses were used to detect the expression of multiple beta-catenin/TCF target genes following aspirin treatment. Aspirin 161-168 catenin beta 1 Homo sapiens 121-133 21721879-5 2011 RESULTS: The transcriptional activity of the beta-catenin/TCF complex was strongly inhibited by aspirin. Aspirin 96-103 catenin beta 1 Homo sapiens 45-57 21721879-8 2011 CONCLUSIONS: The results suggest that aspirin is a potent antitumor agent, and that it exerts its antineoplastic action by inhibition of the beta-catenin/TCF signaling pathway in glioma cells. Aspirin 38-45 catenin beta 1 Homo sapiens 141-153 20188076-1 2010 NO-donating aspirin (NO-ASA, para isomer) has been reported to exhibit strong growth inhibitory effect in Jurkat T-acute lymphoblastic leukemia (T-ALL) cells mediated in part by beta-catenin degradation and caspase activation, but the mechanism(s) still remains unclear. Aspirin 12-19 catenin beta 1 Homo sapiens 178-190 20188076-1 2010 NO-donating aspirin (NO-ASA, para isomer) has been reported to exhibit strong growth inhibitory effect in Jurkat T-acute lymphoblastic leukemia (T-ALL) cells mediated in part by beta-catenin degradation and caspase activation, but the mechanism(s) still remains unclear. Aspirin 24-27 catenin beta 1 Homo sapiens 178-190 19706045-0 2009 Aspirin induces apoptosis in mesenchymal stem cells requiring Wnt/beta-catenin pathway. Aspirin 0-7 catenin beta 1 Homo sapiens 66-78 19706045-8 2009 Stimulating the Wnt/beta-catenin pathway by both Wnt 3a and GSK-3beta inhibitors (LiCl and SB 216763), blocked aspirin-induced apoptosis and protected mitochondrial function, as demonstrated by decreased cytochrome c release and caspase-3 activity. Aspirin 111-118 catenin beta 1 Homo sapiens 20-32 19706045-12 2009 CONCLUSION: These results demonstrate that the Wnt/beta-catenin pathway is a key modulator of aspirin-induced apoptosis in MSCs by regulation of mitochrondrial/caspase-3 function. Aspirin 94-101 catenin beta 1 Homo sapiens 51-63 19576865-3 2009 The p- and m-NO-ASA isomers strongly inhibited cell growth and beta-catenin/TCF transcriptional activity compared to ASA; the IC50s for growth inhibition were 57+/-4, 193+/-10 and >5000microM, and for transcriptional inhibition they were 12+/-1.8, 75+/-6.5 and >5000microM for p-, m-NO-ASA and ASA, respectively. Aspirin 16-19 catenin beta 1 Homo sapiens 63-75 19576865-4 2009 p-NO-ASA reduced the expression of Wnt/beta-catenin downstream target gene cyclin D1, and total cellular beta-catenin levels. Aspirin 5-8 catenin beta 1 Homo sapiens 39-51 19576865-4 2009 p-NO-ASA reduced the expression of Wnt/beta-catenin downstream target gene cyclin D1, and total cellular beta-catenin levels. Aspirin 5-8 catenin beta 1 Homo sapiens 105-117 19026633-3 2009 Furthermore, we demonstrated that the non-steroidal anti-inflammatory drug, sulindac sulfide, the cyclooxygenase-2 (COX-2) selective inhibitor, celecoxib, and the nitric oxide-donating aspirin derivative, NO-ASA, blocked Wnt/beta-catenin signaling in PC-3 and DU145 cells. Aspirin 185-192 catenin beta 1 Homo sapiens 225-237 17357503-0 2006 Down-regulation of beta-catenin nuclear localization by aspirin correlates with growth inhibition of Jurkat cell line. Aspirin 56-63 catenin beta 1 Homo sapiens 19-31 16878161-0 2006 Effect of aspirin on the Wnt/beta-catenin pathway is mediated via protein phosphatase 2A. Aspirin 10-17 catenin beta 1 Homo sapiens 29-41 16878161-3 2006 We studied the effects of aspirin on the oncogenic Wnt/beta-catenin pathway activity in colorectal cancer cell lines and observed that aspirin dose-dependently decreased the activity of this pathway, as judged by TCF-driven luciferase activity, reduced Wnt target gene expression and increased phosphorylation of beta-catenin by immunoblotting. Aspirin 135-142 catenin beta 1 Homo sapiens 55-67 16878161-3 2006 We studied the effects of aspirin on the oncogenic Wnt/beta-catenin pathway activity in colorectal cancer cell lines and observed that aspirin dose-dependently decreased the activity of this pathway, as judged by TCF-driven luciferase activity, reduced Wnt target gene expression and increased phosphorylation of beta-catenin by immunoblotting. Aspirin 135-142 catenin beta 1 Homo sapiens 313-325 16878161-6 2006 Moreover, this inhibition of PP2A enzymatic activity was essential for the effects of aspirin on the Wnt/beta-catenin pathway as shown by transient transfection with PP2A constructs. Aspirin 86-93 catenin beta 1 Homo sapiens 105-117 16895542-10 2006 Western blot analysis demonstrated that the protein level of phosphorylated beta-catenin increased, whereas that of cyclin D1 decreased, after treatment of MSC with aspirin. Aspirin 165-172 catenin beta 1 Homo sapiens 76-88 16895542-13 2006 These observations indicate that aspirin inhibits MSC proliferation and that the downregulation of the wnt/beta-catenin signal pathway may be involved in the growth inhibition of MSC by aspirin. Aspirin 186-193 catenin beta 1 Homo sapiens 107-119 17357503-3 2006 Jurkat cells treated with 3 mmol/L of aspirin could significantly decrease nuclear localization of beta-catenin, and at 5 mmol/L of aspirin, the nuclear localization of beta-catenin was undetectable. Aspirin 38-45 catenin beta 1 Homo sapiens 99-111 17357503-3 2006 Jurkat cells treated with 3 mmol/L of aspirin could significantly decrease nuclear localization of beta-catenin, and at 5 mmol/L of aspirin, the nuclear localization of beta-catenin was undetectable. Aspirin 38-45 catenin beta 1 Homo sapiens 169-181 17357503-3 2006 Jurkat cells treated with 3 mmol/L of aspirin could significantly decrease nuclear localization of beta-catenin, and at 5 mmol/L of aspirin, the nuclear localization of beta-catenin was undetectable. Aspirin 132-139 catenin beta 1 Homo sapiens 169-181 17357503-6 2006 We are led to conclude that aspirin acts through beta-catenin-independent mechanisms. Aspirin 28-35 catenin beta 1 Homo sapiens 49-61 17357503-7 2006 The effects of aspirin include down-regulation of beta-catenin nuclear localization and G0/G1 cell cycle arrest, which might serve as a means of growth inhibition in aspirin-treated human Jurkat cell line. Aspirin 15-22 catenin beta 1 Homo sapiens 50-62 17357503-7 2006 The effects of aspirin include down-regulation of beta-catenin nuclear localization and G0/G1 cell cycle arrest, which might serve as a means of growth inhibition in aspirin-treated human Jurkat cell line. Aspirin 166-173 catenin beta 1 Homo sapiens 50-62 14566053-0 2003 Nitric oxide-donating aspirin inhibits beta-catenin/T cell factor (TCF) signaling in SW480 colon cancer cells by disrupting the nuclear beta-catenin-TCF association. Aspirin 22-29 catenin beta 1 Homo sapiens 39-51 15567157-0 2005 NO-donating aspirin inhibits the growth of leukemic Jurkat cells and modulates beta-catenin expression. Aspirin 12-19 catenin beta 1 Homo sapiens 79-91 15567157-4 2005 The para isomer of NO-ASA degraded beta-catenin in a dose- and time-dependent manner coinciding with increasing expression of activated caspase-3. Aspirin 22-25 catenin beta 1 Homo sapiens 35-47 15567157-5 2005 The caspase inhibitor ZVAD blocked beta-catenin cleavage by p-NO-ASA and partially reversed cell growth inhibition by p-NO-ASA but not that by ASA. Aspirin 65-68 catenin beta 1 Homo sapiens 35-47 14566053-2 2003 We studied the ortho, meta, and para (o-, m-, and p-) positional isomers of NO-donating aspirin (NO-ASA), a chemopreventive agent against colon cancer, for their effect on Beta-catenin/T cell factor (TCF) signaling. Aspirin 88-95 catenin beta 1 Homo sapiens 172-184 16282376-9 2005 NO-ASA disrupted adherens junctions by inducing cleavage of beta- and gamma-catenin, resulting in cell detachment. Aspirin 3-6 catenin beta 1 Homo sapiens 60-83 14566053-0 2003 Nitric oxide-donating aspirin inhibits beta-catenin/T cell factor (TCF) signaling in SW480 colon cancer cells by disrupting the nuclear beta-catenin-TCF association. Aspirin 22-29 catenin beta 1 Homo sapiens 136-148 14566053-3 2003 In human SW480 colon carcinoma cells, cell-growth inhibition by NO-ASA [IC50 values for p-, o-, and m- were 48.1 +/- 4.3 (mean +/-SEM), 60.4 +/- 2.1, and 900 +/-50 microM, respectively] was accompanied by significant inhibition of Beta-catenin signaling. Aspirin 67-70 catenin beta 1 Homo sapiens 231-243 14566053-5 2003 The IC50 values for Beta-catenin/TCF-4-signaling inhibition by NO-ASA were: o-, 2.6 +/- 0.4; m-, 15 +/- 5; p-, 1.1 +/- 0.1 microM; and for ASA, >5,000 microM. Aspirin 66-69 catenin beta 1 Homo sapiens 20-32 12813129-0 2003 Reduction of beta-catenin/T-cell transcription factor signaling by aspirin and indomethacin is caused by an increased stabilization of phosphorylated beta-catenin. Aspirin 67-74 catenin beta 1 Homo sapiens 13-25 14566053-5 2003 The IC50 values for Beta-catenin/TCF-4-signaling inhibition by NO-ASA were: o-, 2.6 +/- 0.4; m-, 15 +/- 5; p-, 1.1 +/- 0.1 microM; and for ASA, >5,000 microM. Aspirin 139-142 catenin beta 1 Homo sapiens 20-32 14566053-7 2003 NO-ASA disrupted the association of Beta-catenin and TCF-4 in the nucleus, whereas ASA did not affect it. Aspirin 3-6 catenin beta 1 Homo sapiens 36-48 12813129-0 2003 Reduction of beta-catenin/T-cell transcription factor signaling by aspirin and indomethacin is caused by an increased stabilization of phosphorylated beta-catenin. Aspirin 67-74 catenin beta 1 Homo sapiens 150-162 12813129-4 2003 Previously, we have shown that the nonsteroidal anti-inflammatory drugs (NSAIDs) aspirin and indomethacin down-regulate beta-catenin/TCF signaling in colorectal cancer cells. Aspirin 81-88 catenin beta 1 Homo sapiens 120-132 12813129-8 2003 The aspirin-induced beta-catenin phosphorylation in colon cancer cells preceded down-regulation of beta-catenin/TCF signaling, suggesting a causal relationship. Aspirin 4-11 catenin beta 1 Homo sapiens 20-32 12813129-8 2003 The aspirin-induced beta-catenin phosphorylation in colon cancer cells preceded down-regulation of beta-catenin/TCF signaling, suggesting a causal relationship. Aspirin 4-11 catenin beta 1 Homo sapiens 99-111 34540977-8 2021 Aspirin has been reported to suppress the Wnt pathway by inducing beta-catenin phosphorylation through the activation of glycogen synthase kinase 3 beta via cyclooxygenase-2 pathway inhibition. Aspirin 0-7 catenin beta 1 Homo sapiens 66-78 11313997-0 2001 The nonsteroidal anti-inflammatory drugs aspirin and indomethacin attenuate beta-catenin/TCF-4 signaling. Aspirin 41-48 catenin beta 1 Homo sapiens 76-88 11313997-4 2001 We therefore investigated beta-catenin/TCF signaling in response to aspirin or indomethacin, respectively, in four CRC cell lines (SW948, SW480, HCT116, LoVo). Aspirin 68-75 catenin beta 1 Homo sapiens 26-38 11313997-5 2001 Both, aspirin and indomethacin inhibited transcription of a beta-catenin/TCF-responsive reporter gene in a dose dependent manner. Aspirin 6-13 catenin beta 1 Homo sapiens 60-72 11313997-10 2001 These results strongly suggest that aspirin and indomethacin attenuate the transcription of beta-catenin/TCF-responsive genes, by modulating TCF activity without disrupting beta-catenin/TCF complex formation. Aspirin 36-43 catenin beta 1 Homo sapiens 92-104