Cited 9 times in
Coupling of LETM1 up-regulation with oxidative phosphorylation and platelet-derived growth factor receptor signaling via YAP1 transactivation
DC Field | Value | Language |
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dc.contributor.author | 김다함 | - |
dc.contributor.author | 이슬기 | - |
dc.contributor.author | 이은직 | - |
dc.contributor.author | 이잔디 | - |
dc.contributor.author | 정웅윤 | - |
dc.contributor.author | 조영석 | - |
dc.contributor.author | 이우경 | - |
dc.date.accessioned | 2017-10-26T07:34:08Z | - |
dc.date.available | 2017-10-26T07:34:08Z | - |
dc.date.issued | 2016 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/152202 | - |
dc.description.abstract | Persistent cellular proliferation and metabolic reprogramming are essential processes in carcinogenesis. Here, we performed Gene Set Enrichment Analysis (GSEA) and found that that LETM1, a mitochondrial calcium transporter, is associated with cellular growth signals such as platelet-derived growth factor (PDGF) receptor signaling and insulin signaling pathways. These results were then verified by qRT-PCR and immnunoblotting. Mechanistically, up-regulation of LETM1 induced YAP1 nuclear accumulation, increasing the expression of PDGFB, PDGFRB and THBS4. Consistent with this, LETM1 silencing caused loss of YAP1 nuclear signal, decreasing the expression of PDGFB, PDGFRB and THBS4. Immunohistochemical staining consistently indicated a positive association between LETM1 up-regulation, YAP1 nuclear localization and high PDGFB expression. In clinical data analysis, LETM1 up-regulation in thyroid cancer was found to be related to aggressive tumor features such as lymphovascular invasion (LVI, P < 0.001) and lymph node metastasis (LNM, P = 0.011). Multivariate analysis demonstrated that LETM1 up-regulation increases the risk of LVI and LNM (OR = 3.455, 95% CI = 1.537-7.766 and OR = 3.043, 95% CI = 1.282-7.225, respectively). Collectively, these data suggest that up-regulation of LETM1 induces sustained activation of proliferative signaling pathways, such as PDGF signal pathway by AKT induced YAP1 transactivation, resulting in aggressive thyroid cancer phenotypes. | - |
dc.description.statementOfResponsibility | open | - |
dc.language | English | - |
dc.publisher | Impact Journals | - |
dc.relation.isPartOf | ONCOTARGET | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Adaptor Proteins, Signal Transducing/genetics | - |
dc.subject.MESH | Adaptor Proteins, Signal Transducing/metabolism* | - |
dc.subject.MESH | Adult | - |
dc.subject.MESH | Calcium-Binding Proteins/genetics | - |
dc.subject.MESH | Calcium-Binding Proteins/metabolism* | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | Female | - |
dc.subject.MESH | Gene Expression Regulation, Neoplastic | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Membrane Proteins/genetics | - |
dc.subject.MESH | Membrane Proteins/metabolism* | - |
dc.subject.MESH | Middle Aged | - |
dc.subject.MESH | Oxidative Phosphorylation* | - |
dc.subject.MESH | Phosphoproteins/genetics | - |
dc.subject.MESH | Phosphoproteins/metabolism* | - |
dc.subject.MESH | RNA Interference | - |
dc.subject.MESH | Receptor, Platelet-Derived Growth Factor beta/genetics | - |
dc.subject.MESH | Receptor, Platelet-Derived Growth Factor beta/metabolism* | - |
dc.subject.MESH | Thyroid Neoplasms/genetics | - |
dc.subject.MESH | Thyroid Neoplasms/metabolism | - |
dc.subject.MESH | Thyroid Neoplasms/pathology | - |
dc.subject.MESH | Transcriptional Activation | - |
dc.subject.MESH | Up-Regulation* | - |
dc.title | Coupling of LETM1 up-regulation with oxidative phosphorylation and platelet-derived growth factor receptor signaling via YAP1 transactivation | - |
dc.type | Article | - |
dc.publisher.location | United States | - |
dc.contributor.college | College of Medicine | - |
dc.contributor.department | Dept. of Internal Medicine | - |
dc.contributor.googleauthor | Jandee Lee | - |
dc.contributor.googleauthor | Woo Kyung Lee | - |
dc.contributor.googleauthor | Mi-Youn Seol | - |
dc.contributor.googleauthor | Seul Gi Lee | - |
dc.contributor.googleauthor | Daham Kim | - |
dc.contributor.googleauthor | Hyunji Kim | - |
dc.contributor.googleauthor | Jongsun Park | - |
dc.contributor.googleauthor | Sang Geun Jung | - |
dc.contributor.googleauthor | Woong Youn Chung | - |
dc.contributor.googleauthor | Eun Jig Lee | - |
dc.contributor.googleauthor | Young Suk Jo | - |
dc.identifier.doi | 10.18632/oncotarget.11456 | - |
dc.contributor.localId | A04626 | - |
dc.contributor.localId | A03050 | - |
dc.contributor.localId | A03066 | - |
dc.contributor.localId | A03674 | - |
dc.contributor.localId | A03853 | - |
dc.contributor.localId | A00363 | - |
dc.contributor.localId | A02991 | - |
dc.relation.journalcode | J02421 | - |
dc.identifier.eissn | 1949-2553 | - |
dc.identifier.pmid | 27556512 | - |
dc.subject.keyword | LETM1 | - |
dc.subject.keyword | cell proliferation | - |
dc.subject.keyword | electron transport chain | - |
dc.subject.keyword | metabolism | - |
dc.subject.keyword | prognosis | - |
dc.contributor.alternativeName | Kim, Da Ham | - |
dc.contributor.alternativeName | Lee, Seul Gi | - |
dc.contributor.alternativeName | Lee, Eun Jig | - |
dc.contributor.alternativeName | Lee, Jan Dee | - |
dc.contributor.alternativeName | Chung, Woung Youn | - |
dc.contributor.alternativeName | Jo, Young Suk | - |
dc.contributor.affiliatedAuthor | Lee, Seul Gi | - |
dc.contributor.affiliatedAuthor | Lee, Eun Jig | - |
dc.contributor.affiliatedAuthor | Lee, Jan Dee | - |
dc.contributor.affiliatedAuthor | Chung, Woung Youn | - |
dc.contributor.affiliatedAuthor | Jo, Young Suk | - |
dc.contributor.affiliatedAuthor | Kim, Da Ham | - |
dc.citation.volume | 7 | - |
dc.citation.number | 41 | - |
dc.citation.startPage | 66728 | - |
dc.citation.endPage | 66739 | - |
dc.identifier.bibliographicCitation | ONCOTARGET , Vol.7(41) : 66728-66739, 2016 | - |
dc.date.modified | 2017-10-24 | - |
dc.identifier.rimsid | 46979 | - |
dc.type.rims | ART | - |
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