Pub. Date : 2018 Sep 20
PMID : 30237564
10 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | In this study, arsenic trioxide (ATO) at 2 muM significantly inhibited the proliferation of the gefitinib-resistant NCI-H1975 cells of the EGFR L858R/T790M mutant compared with a modest inhibition in the gefitinib-sensitive HCC827 cells of DeltaE746-A750 mutant and A549 cells of wild-type EGFR. | Arsenic Trioxide | epidermal growth factor receptor | Homo sapiens |
| 2 | In this study, arsenic trioxide (ATO) at 2 muM significantly inhibited the proliferation of the gefitinib-resistant NCI-H1975 cells of the EGFR L858R/T790M mutant compared with a modest inhibition in the gefitinib-sensitive HCC827 cells of DeltaE746-A750 mutant and A549 cells of wild-type EGFR. | Arsenic Trioxide | epidermal growth factor receptor | Homo sapiens |
| 3 | In this study, arsenic trioxide (ATO) at 2 muM significantly inhibited the proliferation of the gefitinib-resistant NCI-H1975 cells of the EGFR L858R/T790M mutant compared with a modest inhibition in the gefitinib-sensitive HCC827 cells of DeltaE746-A750 mutant and A549 cells of wild-type EGFR. | Arsenic Trioxide | epidermal growth factor receptor | Homo sapiens |
| 4 | In this study, arsenic trioxide (ATO) at 2 muM significantly inhibited the proliferation of the gefitinib-resistant NCI-H1975 cells of the EGFR L858R/T790M mutant compared with a modest inhibition in the gefitinib-sensitive HCC827 cells of DeltaE746-A750 mutant and A549 cells of wild-type EGFR. | Arsenic Trioxide | epidermal growth factor receptor | Homo sapiens |
| 5 | Moreover, ATO significantly inhibited the overall kinase activity of EGFR primarily through quantitatively diminishing the EGFR in NCI-H1975 cells to an extent comparable with that reached by gefitinib in HCC827 cells. | Arsenic Trioxide | epidermal growth factor receptor | Homo sapiens |
| 6 | Moreover, ATO significantly inhibited the overall kinase activity of EGFR primarily through quantitatively diminishing the EGFR in NCI-H1975 cells to an extent comparable with that reached by gefitinib in HCC827 cells. | Arsenic Trioxide | epidermal growth factor receptor | Homo sapiens |
| 7 | Furthermore, ATO promoted autophagic degradation of EGFR in NSCLC cells by directly binding to P62, which interacted with EGFR, preferentially the L858R/T790M mutant providing a plausible explanation for a more favorable effect of ATO on NCI-H1975 cells. | Arsenic Trioxide | epidermal growth factor receptor | Homo sapiens |
| 8 | Furthermore, ATO promoted autophagic degradation of EGFR in NSCLC cells by directly binding to P62, which interacted with EGFR, preferentially the L858R/T790M mutant providing a plausible explanation for a more favorable effect of ATO on NCI-H1975 cells. | Arsenic Trioxide | epidermal growth factor receptor | Homo sapiens |
| 9 | Our results reveal a new target for ATO with a unique molecular mechanism, i.e., ATO suppresses the overall catalytic potential of EGFR, significantly those with the L858R/T790M mutant in NCI-H1975 cells, through an autophagic degradation by interacting with P62. | Arsenic Trioxide | epidermal growth factor receptor | Homo sapiens |
| 10 | Our results reveal a new target for ATO with a unique molecular mechanism, i.e., ATO suppresses the overall catalytic potential of EGFR, significantly those with the L858R/T790M mutant in NCI-H1975 cells, through an autophagic degradation by interacting with P62. | Arsenic Trioxide | epidermal growth factor receptor | Homo sapiens |