PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34886886-0 2021 Roles of reactive oxygen species, mitochondrial membrane potential, and p53 in evodiamine-induced apoptosis and G2/M arrest of human anaplastic thyroid carcinoma cells. evodiamine 79-89 tumor protein p53 Homo sapiens 72-75 34886886-8 2021 Mechanistic studies showed that increased p53 and its downstream proteins, and disrupted MMP with increased intracellular peroxide production participated in EVO-induced apoptosis and G2/M arrest of SW1736 cells. evodiamine 158-161 tumor protein p53 Homo sapiens 42-45 34886886-11 2021 CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells. evodiamine 103-106 tumor protein p53 Homo sapiens 51-54 34886886-11 2021 CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells. evodiamine 103-106 tumor protein p53 Homo sapiens 174-177 34886886-11 2021 CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells. evodiamine 261-264 tumor protein p53 Homo sapiens 51-54 34886886-11 2021 CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells. evodiamine 261-264 tumor protein p53 Homo sapiens 174-177 34886886-11 2021 CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells. evodiamine 299-302 tumor protein p53 Homo sapiens 51-54 27402273-0 2016 A novel alkaloid, evodiamine causes nuclear localization of cytochrome-c and induces apoptosis independent of p53 in human lung cancer cells. evodiamine 18-28 tumor protein p53 Homo sapiens 110-113 31894286-12 2020 In HCT116 cells, Evo increased the phosphorylation of p53, which was enhanced by BMP9 but reduced by BMP9 silencing. evodiamine 17-20 tumor protein p53 Homo sapiens 54-57 31894286-13 2020 Furthermore, the effect of Evo on p53 was potentiated by HIF-1alpha and reduced by HIF-1alpha silencing. evodiamine 27-30 tumor protein p53 Homo sapiens 34-37 31894286-14 2020 The present findings therefore strongly indicated that the anticancer activity of Evo may be partly mediated by BMP9 upregulation, which can activate p53 through upregulation of HIF-1alpha, at least in human colon cancer. evodiamine 82-85 tumor protein p53 Homo sapiens 150-153 30396956-8 2018 In transforming growth factor-beta-treated cells, evodiamine attenuated variations in morphology, growth and migration, and increased p21 and p53 protein levels, and decreased beta-catenin, N-cadherin, vimentin, phospho-AKT, matrix metalloproteinase-2 and matrix metalloproteinase-9 protein levels. evodiamine 50-60 tumor protein p53 Homo sapiens 142-145 31894286-0 2020 BMP9 mediates the anticancer activity of evodiamine through HIF-1alpha/p53 in human colon cancer cells. evodiamine 41-51 tumor protein p53 Homo sapiens 71-74 30384473-8 2018 We found that Evo significantly induced cell cycle arrest at the G2/M phase, upregulated P53 and Bcl-2 associated X proteins (Bax) proteins, and downregulated B-cell lymphoma-2 (Bcl-2), cyclinB1, and cdc2 proteins in HCC cells. evodiamine 14-17 tumor protein p53 Homo sapiens 89-92 27402273-12 2016 Pifithrin-alpha, a p53 inhibitor, slightly inhibited growth of A549 cells and under p53 inhibitory condition evodiamine-induced apoptosis could not be reversed. evodiamine 109-119 tumor protein p53 Homo sapiens 84-87 27402273-13 2016 Together these findings suggest that evodiamine is a strong inducer of apoptosis in lung epithelial cancer cells independent of their p53 status and that could involve both intrinsic as well as extrinsic pathway of apoptosis. evodiamine 37-47 tumor protein p53 Homo sapiens 134-137 26713361-0 2016 Evodiamine selectively targets cancer stem-like cells through the p53-p21-Rb pathway. evodiamine 0-10 tumor protein p53 Homo sapiens 66-69 26713361-7 2016 Surprisingly, evodiamine selectively activated p53 and p21 and decreased inactive Rb, the master molecules in G1/S checkpoint. evodiamine 14-24 tumor protein p53 Homo sapiens 47-50 26580615-9 2015 Taken together, our results suggest that EVO modulates the activity of the p53 signaling pathway to induce apoptosis and downregulate MMP3 expression by inactivating the JAK2/STAT3 pathway through the downregulation of PGI to inhibit migration of HCT-116 human colorectal cancer cells. evodiamine 41-44 tumor protein p53 Homo sapiens 75-78 15821341-2 2005 After treatment with evodiamine for the indicated time periods, anti-apoptotic protein SIRT1 expression was decreased; p53 expression and its phosphorylation were both enhanced, whereas transient induction of downstream p21 was not enough to promote cell cycle arrest. evodiamine 21-31 tumor protein p53 Homo sapiens 119-122 15821341-4 2005 In addition, p53 activation in response to evodiamine administration was correlated with the activation of the PI3-K/PKC pro-apoptotic pathway, but did not require ERK participation. evodiamine 43-53 tumor protein p53 Homo sapiens 13-16