PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33667788-5 2021 Paclitaxel, doxorubicin, tamoxifen, erlotinib, gefitinib, temozolomide, and methotrexate are among therapeutic agents whose efficacy is influenced by the expression of H19. Doxorubicin 12-23 H19 imprinted maternally expressed transcript Homo sapiens 168-171 32345117-8 2020 We observed that the H19 expression was significantly upregulated in chemotherapy-resistant breast cancer tissues and doxorubicin-resistant breast cancer cell lines. Doxorubicin 118-129 H19 imprinted maternally expressed transcript Homo sapiens 21-24 32345117-9 2020 Knockdown of H19 enhanced the sensitivity to doxorubicin both in vitro and in vivo. Doxorubicin 45-56 H19 imprinted maternally expressed transcript Homo sapiens 13-16 32345117-10 2020 While H19 overexpression developed doxorubicin-resistant in breast cancer cells both in vitro and in vivo. Doxorubicin 35-46 H19 imprinted maternally expressed transcript Homo sapiens 6-9 32345117-11 2020 Furthermore, it was revealed that H19 negatively regulated PARP1 expression in breast cancer cells following doxorubicin treatment. Doxorubicin 109-120 H19 imprinted maternally expressed transcript Homo sapiens 34-37 32345117-12 2020 Knockdown of H19 sensitized breast cancer cells to doxorubicin by promoting PARP1 upregulation. Doxorubicin 51-62 H19 imprinted maternally expressed transcript Homo sapiens 13-16 32345117-13 2020 H19 overexpression could recapitulate doxorubicin resistance by PARP1 downregulation. Doxorubicin 38-49 H19 imprinted maternally expressed transcript Homo sapiens 0-3 32345117-0 2020 Long non-coding RNA H19 regulates proliferation and Doxorubicin resistance in MCF-7 cells by targeting PARP1. Doxorubicin 52-63 H19 imprinted maternally expressed transcript Homo sapiens 20-23 32345117-3 2020 The long noncoding RNA H19 (H19) is involved in various stages of tumorigenesis, however, its role in doxorubicin resistance remains unknown. Doxorubicin 102-113 H19 imprinted maternally expressed transcript Homo sapiens 23-26 32345117-3 2020 The long noncoding RNA H19 (H19) is involved in various stages of tumorigenesis, however, its role in doxorubicin resistance remains unknown. Doxorubicin 102-113 H19 imprinted maternally expressed transcript Homo sapiens 28-31 32345117-4 2020 The goal of this study was to evaluate the role of H19 in the development of doxorubicin-resistant breast cancer. Doxorubicin 77-88 H19 imprinted maternally expressed transcript Homo sapiens 51-54 32345117-6 2020 Both knockdown and overexpression of H19 were used to assess the sensitivity to doxorubicin in breast cancer cells in vitro and in vivo. Doxorubicin 80-91 H19 imprinted maternally expressed transcript Homo sapiens 37-40 32345117-7 2020 qRT-PCR and Western blot were used to explore the doxorubicin resistance mechanism of H19. Doxorubicin 50-61 H19 imprinted maternally expressed transcript Homo sapiens 86-89 29190892-0 2017 LncRNA H19 is a major mediator of doxorubicin chemoresistance in breast cancer cells through a cullin4A-MDR1 pathway. Doxorubicin 34-45 H19 imprinted maternally expressed transcript Homo sapiens 7-10 29190892-3 2017 In the present study, we investigated the role and molecular mechanism of H19 lncRNA in chemoresistance development by using doxorubicin (Dox) resistance in breast cancer cells as a model system. Doxorubicin 125-136 H19 imprinted maternally expressed transcript Homo sapiens 74-77 29190892-3 2017 In the present study, we investigated the role and molecular mechanism of H19 lncRNA in chemoresistance development by using doxorubicin (Dox) resistance in breast cancer cells as a model system. Doxorubicin 138-141 H19 imprinted maternally expressed transcript Homo sapiens 74-77 29190892-4 2017 H19 lncRNA expression was significantly increased in anthracycline-treated and Dox-resistant MCF-7 breast cancer cells. Doxorubicin 79-82 H19 imprinted maternally expressed transcript Homo sapiens 0-3 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Doxorubicin 153-156 H19 imprinted maternally expressed transcript Homo sapiens 5-8 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Doxorubicin 153-156 H19 imprinted maternally expressed transcript Homo sapiens 115-118 29190892-5 2017 This H19 overexpression was contributed to cancer cell resistance to anthracyclines and paclitaxel as knockdown of H19 lncRNA by a specific H19 shRNA in Dox-resistant cells significantly improved the cell sensitivity to anthracyclines and paclitaxel. Doxorubicin 153-156 H19 imprinted maternally expressed transcript Homo sapiens 115-118 29190892-6 2017 Furthermore, gene expression profiling analysis revealed that a total of 192 genes were associated with H19-mediated Dox resistance. Doxorubicin 117-120 H19 imprinted maternally expressed transcript Homo sapiens 104-107 29190892-8 2017 Using genetic and pharmacological approaches, we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down. Doxorubicin 119-122 H19 imprinted maternally expressed transcript Homo sapiens 105-108 29190892-8 2017 Using genetic and pharmacological approaches, we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down. Doxorubicin 119-122 H19 imprinted maternally expressed transcript Homo sapiens 262-265 29190892-8 2017 Using genetic and pharmacological approaches, we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down. Doxorubicin 210-213 H19 imprinted maternally expressed transcript Homo sapiens 105-108 29190892-8 2017 Using genetic and pharmacological approaches, we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down. Doxorubicin 210-213 H19 imprinted maternally expressed transcript Homo sapiens 262-265 31225433-6 2017 Clonogenicity and proliferation assays showed that H19 overexpression could suppress tumor cell survival and proliferation after treatment with either sorafenib or doxorubicin, suggesting chemosensitizing actions of H19. Doxorubicin 164-175 H19 imprinted maternally expressed transcript Homo sapiens 51-54 31225433-10 2017 Chemoresistant cells were sensitized after H19 overexpression by either increasing the cytotoxic action of doxorubicin or decreasing cell proliferation upon sorafenib treatment. Doxorubicin 107-118 H19 imprinted maternally expressed transcript Homo sapiens 43-46 31994191-0 2020 Exosome-mediated transfer of long noncoding RNA H19 induces doxorubicin resistance in breast cancer. Doxorubicin 60-71 H19 imprinted maternally expressed transcript Homo sapiens 48-51 31994191-3 2020 In this study, the role of long noncoding RNA H19 within exosomes is elucidated in terms of regulating doxorubicin (DOX) resistance of breast cancer. Doxorubicin 103-114 H19 imprinted maternally expressed transcript Homo sapiens 46-49 31994191-3 2020 In this study, the role of long noncoding RNA H19 within exosomes is elucidated in terms of regulating doxorubicin (DOX) resistance of breast cancer. Doxorubicin 116-119 H19 imprinted maternally expressed transcript Homo sapiens 46-49 31994191-4 2020 As a result, increased H19 expression was observed in DOX-resistant breast cancer cells in comparison with the corresponding parental cells. Doxorubicin 54-57 H19 imprinted maternally expressed transcript Homo sapiens 23-26 31994191-5 2020 Suppression of H19 significantly lowered DOX resistance by decreasing cell viability, lowering colony-forming ability, and inducing apoptosis. Doxorubicin 41-44 H19 imprinted maternally expressed transcript Homo sapiens 15-18 31994191-8 2020 Taken together, H19 could be delivered by exosomes to sensitive cells, leading to the dissemination of DOX resistance. Doxorubicin 103-106 H19 imprinted maternally expressed transcript Homo sapiens 16-19 31994191-9 2020 Our finding highlights the potential of exosomal H19 as a molecular target to reduce DOX resistance. Doxorubicin 85-88 H19 imprinted maternally expressed transcript Homo sapiens 49-52 17297456-4 2007 H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. Doxorubicin 136-147 H19 imprinted maternally expressed transcript Homo sapiens 0-3 17297456-4 2007 H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. Doxorubicin 136-147 H19 imprinted maternally expressed transcript Homo sapiens 45-48 17297456-4 2007 H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. Doxorubicin 182-193 H19 imprinted maternally expressed transcript Homo sapiens 0-3 17297456-4 2007 H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. Doxorubicin 182-193 H19 imprinted maternally expressed transcript Homo sapiens 45-48