PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28609310-0 2017 Blockade of GLUT1 by WZB117 resensitizes breast cancer cells to adriamycin. Doxorubicin 64-74 solute carrier family 2 member 1 Homo sapiens 12-17 33096154-3 2020 Accordingly, several studies on combining glucose transporter (GLUT) inhibitors with chemotherapeutic agents, such as doxorubicin, paclitaxel, and cytarabine, showed synergistic or additive anticancer effects, reduced chemo-, radio-, and immuno-resistance, and reduced toxicity due to lowering the therapeutic doses required for desired chemotherapeutic effects, as compared with monotherapy. Doxorubicin 118-129 solute carrier family 2 member 1 Homo sapiens 42-61 33096154-3 2020 Accordingly, several studies on combining glucose transporter (GLUT) inhibitors with chemotherapeutic agents, such as doxorubicin, paclitaxel, and cytarabine, showed synergistic or additive anticancer effects, reduced chemo-, radio-, and immuno-resistance, and reduced toxicity due to lowering the therapeutic doses required for desired chemotherapeutic effects, as compared with monotherapy. Doxorubicin 118-129 solute carrier family 2 member 1 Homo sapiens 63-67 29031537-0 2018 Silybin counteracts doxorubicin resistance by inhibiting GLUT1 expression. Doxorubicin 20-31 solute carrier family 2 member 1 Homo sapiens 57-62 29031537-6 2018 Moreover, both GLUT1 mRNA and protein expression significantly increased in LoVo DOX cells. Doxorubicin 81-84 solute carrier family 2 member 1 Homo sapiens 15-20 28609310-2 2017 In the present study, we explored whether inhibiting the glucose transporter 1 (GLUT1) could restore the activity of adriamycin in breast cancer cell line MCF-7 resistant to adriamycin and the possible underlying mechanisms. Doxorubicin 117-127 solute carrier family 2 member 1 Homo sapiens 57-78 28609310-2 2017 In the present study, we explored whether inhibiting the glucose transporter 1 (GLUT1) could restore the activity of adriamycin in breast cancer cell line MCF-7 resistant to adriamycin and the possible underlying mechanisms. Doxorubicin 117-127 solute carrier family 2 member 1 Homo sapiens 80-85 28609310-2 2017 In the present study, we explored whether inhibiting the glucose transporter 1 (GLUT1) could restore the activity of adriamycin in breast cancer cell line MCF-7 resistant to adriamycin and the possible underlying mechanisms. Doxorubicin 174-184 solute carrier family 2 member 1 Homo sapiens 57-78 28609310-2 2017 In the present study, we explored whether inhibiting the glucose transporter 1 (GLUT1) could restore the activity of adriamycin in breast cancer cell line MCF-7 resistant to adriamycin and the possible underlying mechanisms. Doxorubicin 174-184 solute carrier family 2 member 1 Homo sapiens 80-85 28609310-3 2017 Adriamycin-resistant cell line MCF-7/ADR was selected stepwise from the parental MCF-7 cells and the level of GLUT1 was measured. Doxorubicin 0-10 solute carrier family 2 member 1 Homo sapiens 110-115 27569031-9 2016 Compared to non-targeted micelles, GLUT1 scFv surface modification increased the association of micelles (>20%, P<0.01) and the nuclear localization of doxorubicin (~3-fold) in U87MGcells, which also translated into enhanced cytotoxicity. Doxorubicin 158-169 solute carrier family 2 member 1 Homo sapiens 35-40 28609310-8 2017 Inhibition of the GLUT1 could partially restore the antineoplastic effects of adriamycin in the adriamycin-resistant MCF-7 cell line possibly through activating the AMPK, downregulating the mTOR pathway, and increasing the BAX translocation to mitochondria. Doxorubicin 78-88 solute carrier family 2 member 1 Homo sapiens 18-23 28609310-8 2017 Inhibition of the GLUT1 could partially restore the antineoplastic effects of adriamycin in the adriamycin-resistant MCF-7 cell line possibly through activating the AMPK, downregulating the mTOR pathway, and increasing the BAX translocation to mitochondria. Doxorubicin 96-106 solute carrier family 2 member 1 Homo sapiens 18-23 24467213-7 2014 Subsequent functional experiments based on RNA interference technology showed that CTSD, FKBP10, and SLC2A1 are novel genes that participate in the acquisition and maintenance of the adriamycin-resistant phenotype in leukemia cells. Doxorubicin 183-193 solute carrier family 2 member 1 Homo sapiens 101-107 24641416-7 2014 Down-regulation of the expression of GLUT1 by RNA interference obviously sensitized drug-resistant HL-60/ADR cells to adriamycin (ADR) in vitro, comparable with RNA interference for the HIF-1alpha gene. Doxorubicin 118-128 solute carrier family 2 member 1 Homo sapiens 37-42 25101238-6 2014 Mutation of an ATM target site on GLUT1 (GLUT1-S490A) increased ROS levels and prevented the ROS-lowering effect of the ATM activator doxorubicin. Doxorubicin 134-145 solute carrier family 2 member 1 Homo sapiens 34-39 25101238-6 2014 Mutation of an ATM target site on GLUT1 (GLUT1-S490A) increased ROS levels and prevented the ROS-lowering effect of the ATM activator doxorubicin. Doxorubicin 134-145 solute carrier family 2 member 1 Homo sapiens 41-46 20870738-3 2010 Here, we report that DNA-damaging anticancer agents such as Adriamycin and etoposide suppressed the expression of GLUT3, but not GLUT1, in HeLa cells and a tumorigenic HeLa cell hybrid. Doxorubicin 60-70 solute carrier family 2 member 1 Homo sapiens 129-134 24098980-0 2013 Anti-cancer activity of anti-GLUT1 antibody-targeted polymeric micelles co-loaded with curcumin and doxorubicin. Doxorubicin 100-111 solute carrier family 2 member 1 Homo sapiens 29-34 24098980-4 2013 METHODS: HCT-116 cells were treated with non-targeted and GLUT1-targeted CUR and DOX micelles as a single agent or in combination. Doxorubicin 81-84 solute carrier family 2 member 1 Homo sapiens 58-63 24098980-7 2013 RESULTS: CUR + DOX-loaded micelles decorated with GLUT1 had a robust killing effect even at low doses of DOX in vitro. Doxorubicin 15-18 solute carrier family 2 member 1 Homo sapiens 50-55 24098980-7 2013 RESULTS: CUR + DOX-loaded micelles decorated with GLUT1 had a robust killing effect even at low doses of DOX in vitro. Doxorubicin 105-108 solute carrier family 2 member 1 Homo sapiens 50-55 24098980-9 2013 However, GLUT1-CUR and GLUT1-CUR + DOX micelles showed a significant tumor inhibition effect with an improvement in survival. Doxorubicin 35-38 solute carrier family 2 member 1 Homo sapiens 23-28 24098980-11 2013 Hence, we confirmed that GLUT1-CUR + DOX micelles are effective and deserve further investigation. Doxorubicin 37-40 solute carrier family 2 member 1 Homo sapiens 25-30 16595493-10 2006 With DOX treatment, the cells showed increased Glut-1 mRNA and decreased HKII mRNA for the duration of active treatment; these levels returned to those seen in the untreated cells once the treatment was stopped for 24 h. However, HKII protein levels remained somewhat low. Doxorubicin 5-8 solute carrier family 2 member 1 Homo sapiens 47-53 16595493-12 2006 CONCLUSION: After DOX or 5FU therapy, the relationship between (3)H-FDG uptake and viable cell number can become disjointed, with transient declines in (3)H-FDG uptake in excess of the decline in cell number despite increased Glut-1 mRNA levels. Doxorubicin 18-21 solute carrier family 2 member 1 Homo sapiens 226-232 16595493-3 2006 Glucose transporter-1 (Glut-1) and hexokinase II (HKII) proteins are highly expressed in many breast carcinomas, but their status while undergoing DOX or 5FU chemotherapy has not been systematically evaluated. Doxorubicin 147-150 solute carrier family 2 member 1 Homo sapiens 0-21 16595493-3 2006 Glucose transporter-1 (Glut-1) and hexokinase II (HKII) proteins are highly expressed in many breast carcinomas, but their status while undergoing DOX or 5FU chemotherapy has not been systematically evaluated. Doxorubicin 147-150 solute carrier family 2 member 1 Homo sapiens 23-29