Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이윤실 | * |
dc.date.accessioned | 2016-08-27T04:08:04Z | - |
dc.date.available | 2016-08-27T04:08:04Z | - |
dc.date.issued | 2016 | * |
dc.identifier.issn | 1949-2553 | * |
dc.identifier.other | OAK-18370 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/218133 | - |
dc.description.abstract | MicroRNA array analysis revealed that miR-217 expression was decreased in anti-cancer drug-resistant Malme3M(R) cancer cells. CAGE, a cancer/testis antigen, was predicted as a target of miR-217. Luciferase activity and ChIP assays revealed a negative feedback relationship between CAGE and miR-217. miR-217 and CAGE oppositely regulated the response to anti-cancer drugs such as taxol, gefitinib and trastuzumab, an inhibitor of HER2. miR-217 negatively regulated the tumorigenic, metastatic, angiogenic, migration and invasion potential of cancer cells. The xenograft of Malme3M(R) cells showed an increased expression of pEGFRY845. CAGE and miR-217 inhibitor regulated the expression of pEGFRY845. CAGE showed interactions with EGFR and HER2 and regulated the in vivo sensitivity to trastuzumab. The down-regulation of EGFR or HER2 enhanced the sensitivity to anti-cancer drugs. CAGE showed direct regulation of HER2 and was necessary for the interaction between EGFR and HER2 in Malme3M(R) cells. miR-217 inhibitor induced interactions of CAGE with EGFR and HER2 in Malme3M cells. The inhibition of EGFR by CAGE-binding GTGKT peptide enhanced the sensitivity to gefitinib and trastuzumab and prevented interactions of EGFR with CAGE and HER2. Our results show that miR-217-CAGE feedback loop serves as a target for overcoming resistance to various anti-cancer drugs, including EGFR and HER2 inhibitors. | * |
dc.language | English | * |
dc.publisher | IMPACT JOURNALS LLC | * |
dc.subject | anti-cancer drug-resistance | * |
dc.subject | CAGE | * |
dc.subject | EGFR | * |
dc.subject | HER2 | * |
dc.subject | miR-217 | * |
dc.title | miR-217 and CAGE form feedback loop and regulates the response to anti-cancer drugs through EGFR and HER2 | * |
dc.type | Article | * |
dc.relation.issue | 9 | * |
dc.relation.volume | 7 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 10297 | * |
dc.relation.lastpage | 10321 | * |
dc.relation.journaltitle | ONCOTARGET | * |
dc.identifier.wosid | WOS:000375672900052 | * |
dc.identifier.scopusid | 2-s2.0-84961620619 | * |
dc.author.google | Kim, Youngmi | * |
dc.author.google | Kim, Hyuna | * |
dc.author.google | Park, Deokbum | * |
dc.author.google | Han, Minho | * |
dc.author.google | Lee, Hansoo | * |
dc.author.google | Lee, Yun Sil | * |
dc.author.google | Choe, Jongseon | * |
dc.author.google | Kim, Young Myeong | * |
dc.author.google | Jeoung, Dooil | * |
dc.contributor.scopusid | 이윤실(17137192000) | * |
dc.date.modifydate | 20240130115944 | * |