Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 신인철 | - |
dc.date.accessioned | 2019-11-25T01:14:27Z | - |
dc.date.available | 2019-11-25T01:14:27Z | - |
dc.date.issued | 2017-05 | - |
dc.identifier.citation | ONCOTARGET, v. 8, no. 22, page. 35804-35823 | en_US |
dc.identifier.issn | 1949-2553 | - |
dc.identifier.uri | http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=16208&path[]=51849 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/113935 | - |
dc.description.abstract | Galectin-1 is a beta-galactoside binding protein secreted by many types of aggressive cancer cells. Although many studies have focused on the role of galectin-1 in cancer progression, relatively little attention has been paid to galectin-1 as an extracellular therapeutic target. To elucidate the molecular mechanisms underlying galectin-1-mediated cancer progression, we established galectin-1 knock-down cells via retroviral delivery of short hairpin RNA (shRNA) against galectin-1 in two triple-negative breast cancer (TNBC) cell lines, MDA-MB-231 and Hs578T. Ablation of galectin-1 expression decreased cell proliferation, migration, invasion, and doxorubicin resistance. We found that these effects were caused by decreased galectin-1-integrin 1 interactions and suppression of the downstream focal adhesion kinase (FAK)/cSrc pathway. We also found that silencing of galectin-1 inhibited extracellular signalregulated kinase (ERK)/signal transducer and activator of transcription 3 (STAT3) signaling, thereby down-regulating survivin expression. This finding implicates STAT3 as a transcription factor for survivin. Finally, rescue of endogenous galectin-1 knockdown and recombinant galectin-1 treatment both recovered signaling through the FAK/c-Src/ERK/STAT3/survivin pathway. Taken together, these results suggest that extracellular galectin-1 contributes to cancer progression and doxorubicin resistance in TNBC cells. These effects appear to be mediated by galectin-1-induced up-regulation of the integrin beta 1/FAK/c-Src/ERK/STAT3/survivin pathway. Our results imply that extracellular galectin-1 has potential as a therapeutic target for triple-negative breast cancer. | en_US |
dc.description.sponsorship | This work was supported by an NRF grant (2016R1A2B4011196) from the Korea Research Foundation. | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | IMPACT JOURNALS LLC | en_US |
dc.subject | galectin-1 | en_US |
dc.subject | integrin beta 1 | en_US |
dc.subject | STAT3 | en_US |
dc.subject | survivin | en_US |
dc.subject | drug resistance | en_US |
dc.title | Binding of galectin-1 to integrin beta 1 potentiates drug resistance by promoting survivin expression in breast cancer cells | en_US |
dc.type | Article | en_US |
dc.relation.no | 22 | - |
dc.relation.volume | 8 | - |
dc.identifier.doi | 10.18632/oncotarget.16208 | - |
dc.relation.page | 35804-35823 | - |
dc.relation.journal | ONCOTARGET | - |
dc.contributor.googleauthor | Nam, KeeSoo | - |
dc.contributor.googleauthor | Son, Seog-Ho | - |
dc.contributor.googleauthor | Oh, Sunhwa | - |
dc.contributor.googleauthor | Jeon, Donghwan | - |
dc.contributor.googleauthor | Kim, Hyungjoo | - |
dc.contributor.googleauthor | Noh, Dong-Young | - |
dc.contributor.googleauthor | Kim, Sangmin | - |
dc.contributor.googleauthor | Shin, Incheol | - |
dc.relation.code | 2017009424 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF NATURAL SCIENCES[S] | - |
dc.sector.department | DEPARTMENT OF LIFE SCIENCE | - |
dc.identifier.pid | incheol | - |
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