PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19840446-5 2009 It is concluded that the TET possesses the reversal effect on multiple drug resistance of K562/A02 cells with concentration dependence, the reversal effect of TET may be related to up-regulation of P21 expression and down-regulation of P-gp and mdr-1 gene expressions in K562/A02 cells. tet 159-162 ATP binding cassette subfamily B member 1 Homo sapiens 245-250 9625436-3 1998 TET (3.0 microM), FAN (3.0 microM) and VER (10.0 microM) reduced the paclitaxel (TAX) concentration required to achieve 50% inhibition of cell growth (EC50) to HCT15 (P-gp-positive) cells about 3100-, 1900- and 410-fold, and these compounds also reduced the EC50 value of actinomycin D (AMD) about 36.0-, 45.9- and 18.2-fold in the cells, respectively. tet 0-3 ATP binding cassette subfamily B member 1 Homo sapiens 167-171 9625436-5 1998 On the other hand, TET (3.0 microM), FAN (3.0 microM) and VER (10.0 microM) similarly enhanced the accumulation rates of rhodamine 123, a well known P-gp substrate, in HCT15 cells (200-250%). tet 19-22 ATP binding cassette subfamily B member 1 Homo sapiens 149-153 9625436-8 1998 From the result, we conclude that TET and FAN enhanced the cytotoxicity of MDR-related drugs via modulation of P-gp. tet 34-37 ATP binding cassette subfamily B member 1 Homo sapiens 111-115 28260091-5 2017 The cells treated with paclitaxel alone eventually acquired MDR along with the overexpression of and highly activated P-glycoprotein (Pgp), while the cells treated with the paclitaxel-TET combination were sensitive to chemotherapeutic drugs and expressed decreased levels of Pgp and less Pgp activity. tet 184-187 ATP binding cassette subfamily B member 1 Homo sapiens 275-278 28260091-5 2017 The cells treated with paclitaxel alone eventually acquired MDR along with the overexpression of and highly activated P-glycoprotein (Pgp), while the cells treated with the paclitaxel-TET combination were sensitive to chemotherapeutic drugs and expressed decreased levels of Pgp and less Pgp activity. tet 184-187 ATP binding cassette subfamily B member 1 Homo sapiens 275-278 28260091-9 2017 On the whole, our findings suggest that TET prevents paclitaxel-induced MDR by inhibiting Pgp overexpression through a mechanism that may involve the inhibition of NF-kappaB signaling in osteosarcoma. tet 40-43 ATP binding cassette subfamily B member 1 Homo sapiens 90-93 24520791-8 2014 Positive correlation existed between ZNF139 and MRP-1, ZNF139 and MDR1 before treated by TET in SGC7901/ADR, and this relationship also existed in SGC7901/ADR cells after treated by TET (all P < 0.05). tet 89-92 ATP binding cassette subfamily B member 1 Homo sapiens 66-70 24520791-8 2014 Positive correlation existed between ZNF139 and MRP-1, ZNF139 and MDR1 before treated by TET in SGC7901/ADR, and this relationship also existed in SGC7901/ADR cells after treated by TET (all P < 0.05). tet 182-185 ATP binding cassette subfamily B member 1 Homo sapiens 66-70 24520791-9 2014 CONCLUSION: TET could achieve MDR reversion in gastric cancer cells by down-regulating the expression of ZNF139, MRP-1, and MDR1. tet 12-15 ATP binding cassette subfamily B member 1 Homo sapiens 124-128 19840446-5 2009 It is concluded that the TET possesses the reversal effect on multiple drug resistance of K562/A02 cells with concentration dependence, the reversal effect of TET may be related to up-regulation of P21 expression and down-regulation of P-gp and mdr-1 gene expressions in K562/A02 cells. tet 25-28 ATP binding cassette subfamily B member 1 Homo sapiens 245-250