https://scholars.lib.ntu.edu.tw/handle/123456789/465677
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | Syu J.-P. | en_US |
dc.contributor.author | Chi J.-T. | en_US |
dc.contributor.author | HSIU-NI KUNG | en_US |
dc.creator | HSIU-NI KUNG;Chi J.-T.;Syu J.-P. | - |
dc.date.accessioned | 2020-02-27T06:20:45Z | - |
dc.date.available | 2020-02-27T06:20:45Z | - |
dc.date.issued | 2016 | - |
dc.identifier.issn | 1949-2553 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84962788166&doi=10.18632%2foncotarget.7406&partnerID=40&md5=09d55468db851994058f02d2ee2efca9 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/465677 | - |
dc.description.abstract | Hypoxia leads to reactive oxygen species (ROS) imbalance, which is proposed to associate with drug resistance and oncogenesis. Inhibition of enzymes of antioxidant balancing system in tumor cells was shown to reduce chemoresistance under hypoxia. However, the underlying mechanism remains unknown. The key regulator of antioxidant balancing system is nuclear factor erythroid 2-related factor 2 (NFE2L2, Nrf2). In this study, we showed that hypoxia induced ROS production and increased the Nrf2 activity. Nrf2 activation increased levels of its downstream target antioxidant enzymes, including GCLC and GCLM. The Nrf2-overexpressing also confers chemo-resistant MCF7 cells under normoxia. The in vivo mouse model also demonstrated that the chemical inhibition of Nrf2 can increase cisplatin (CDDP) cytotoxicity. Together, these results showed that Nrf2 serves as a key regulator in chemotherapeutic resistance under hypoxia through ROS-Nrf2-GCLC-GSH pathway. Therefore, targeting Nrf2 can be a potential treatment for hypoxia-induced drug resistance in breast cancer cells. | - |
dc.publisher | Impact Journals LLC | - |
dc.relation.ispartof | Oncotarget | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | cisplatin; glutamate cysteine ligase; glutamate cysteine ligase catalytic subunit; glutamate cysteine ligase modifier subunit; glutathione; reactive oxygen metabolite; transcription factor Nrf2; unclassified drug; antineoplastic agent; cisplatin; GCLC protein, human; glutamate cysteine ligase; glutamate-cysteine ligase modifier subunit, human; NFE2L2 protein, human; transcription factor Nrf2; tumor marker; animal experiment; animal model; animal tissue; Article; breast cancer; cancer resistance; cancer survival; controlled study; enzyme activity; enzyme assay; human; hypoxia; in vivo study; male; MCF 7 cell line; molecular dynamics; mouse; nonhuman; protein determination; protein expression; protein function; protein targeting; signal transduction; survival rate; animal; apoptosis; breast tumor; cell proliferation; drug resistance; drug screening; female; gene expression regulation; genetics; Institute for Cancer Research mouse; metabolism; pathology; pathophysiology; tumor cell culture; Animals; Antineoplastic Agents; Apoptosis; Biomarkers, Tumor; Breast Neoplasms; Cell Proliferation; Cisplatin; Drug Resistance, Neoplasm; Female; Gene Expression Regulation, Neoplastic; Glutamate-Cysteine Ligase; Humans; Hypoxia; Mice; Mice, Inbred ICR; NF-E2-Related Factor 2; Signal Transduction; Tumor Cells, Cultured; Xenograft Model Antitumor Assays | - |
dc.title | Nrf2 is the key to chemotherapy resistance in MCF7 breast cancer cells under hypoxia | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.18632/oncotarget.7406 | - |
dc.identifier.pmid | 26894974 | - |
dc.identifier.scopus | 2-s2.0-84962788166 | - |
dc.relation.pages | 14659-14672 | - |
dc.relation.journalvolume | 7 | - |
dc.relation.journalissue | 12 | - |
item.fulltext | no fulltext | - |
item.openairetype | journal article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | Anatomy and Cell Biology | - |
crisitem.author.orcid | 0000-0001-6979-8346 | - |
crisitem.author.parentorg | College of Medicine | - |
顯示於: | 解剖學暨細胞生物學科所 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。