PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33747224-11 2021 Moreover, overexpression of miR-26a significantly suppressed cell proliferation, clone formation ability and metastasis, and it sensitized breast cancer cells to docetaxel. Docetaxel 162-171 microRNA 26a-1 Homo sapiens 28-35 28214878-10 2017 Xenograft transplantation, immunohistochemistry, tunel assays and western blotting assays were employed to demonstrate the role of miR-26a in docetaxel resistant LAD cells in vivo. Docetaxel 142-151 microRNA 26a-1 Homo sapiens 131-138 28214878-14 2017 RESULTS: MiR-26a was significantly down-regulated in the dcetaxel-insensitive groups (n = 19) compared with the docetaxel-sensitive groups (n = 18) assessed by qRT-PCR. Docetaxel 112-121 microRNA 26a-1 Homo sapiens 9-16 28214878-15 2017 MiR-26a decreased the proliferation, increased the apoptosis rate and reversed EMT to MET of docetaxel-resistant LAD cells both in vivo and vitro. Docetaxel 93-102 microRNA 26a-1 Homo sapiens 0-7 28214878-17 2017 Rescue assays further verified that the function of miR-26a exerts in docetaxel-resistant LAD cells is through targeting EZH2. Docetaxel 70-79 microRNA 26a-1 Homo sapiens 52-59 28214878-18 2017 CONCLUSIONS: Our data revealed that overexpression of miR-26a in docetaxel-resistant LAD cells could decrease the proliferation, increase the apoptosis rate and reverse EMT to MET of docetaxel-resistant LAD cells both in vivo and vitro and such function is partially exerted via downregulating EZH2. Docetaxel 65-74 microRNA 26a-1 Homo sapiens 54-61 28214878-18 2017 CONCLUSIONS: Our data revealed that overexpression of miR-26a in docetaxel-resistant LAD cells could decrease the proliferation, increase the apoptosis rate and reverse EMT to MET of docetaxel-resistant LAD cells both in vivo and vitro and such function is partially exerted via downregulating EZH2. Docetaxel 183-192 microRNA 26a-1 Homo sapiens 54-61 28214878-19 2017 MiR-26a/EZH2 signal pathway makes contribute to the malignant phenotype of docetaxel-resistant of LAD cells which indicated that miR-26a exerts pivotal functions in the molecular etiology of chemoresistant lung adenocarcinoma. Docetaxel 75-84 microRNA 26a-1 Homo sapiens 0-7 28214878-19 2017 MiR-26a/EZH2 signal pathway makes contribute to the malignant phenotype of docetaxel-resistant of LAD cells which indicated that miR-26a exerts pivotal functions in the molecular etiology of chemoresistant lung adenocarcinoma. Docetaxel 75-84 microRNA 26a-1 Homo sapiens 129-136