Cited 44 times in
Functional invadopodia formation through stabilization of the PDPN transcript by IMP-3 and cancer-stromal crosstalk for PDPN expression.
DC Field | Value | Language |
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dc.contributor.author | 박광균 | - |
dc.contributor.author | 장향란 | - |
dc.contributor.author | 정원윤 | - |
dc.contributor.author | 황영선 | - |
dc.date.accessioned | 2014-12-19T16:37:34Z | - |
dc.date.available | 2014-12-19T16:37:34Z | - |
dc.date.issued | 2012 | - |
dc.identifier.issn | 0143-3334 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/89883 | - |
dc.description.abstract | We previously reported that insulin-like growth factor-II mRNA-binding protein-3 (IMP-3) depletion (IMP-3(Δ)) was shown to inhibit invadopodia formation and extracellular matrix degradation capacity in oral squamous cell carcinoma (OSCC) cells. In this study, we found that IMP-3(Δ) cells significantly downregulated the podoplanin (PDPN) level, which resulted in a loss of extracellular matrix degradation activity, although invadopodia was still thriving. From RNA in situ hybridization using a digoxigenin-labeled 3'UTR recognition probe of PDPN and reporter assay with 3'UTR of the PDPN gene cloned downstream from the luciferase reporter gene, we revealed that IMP-3 depletion was shown to be downregulated, which most probably lowered PDPN gene expression by reducing mRNA stabilization. In a xenograft model, PDPN depletion was the cause of a decrease in tumor volume and regional infiltration into nearby stroma. Taken together, transforming growth factor beta 1 increased PDPN expression, which potentiated cancer invasion through increased invadopodia formation and extracellular matrix degradation in the low invasive OSCC cell line. Reciprocally, interleukin-1 beta secreted by OSCC cells, stimulated transforming growth factor beta 1 secretion from stromal fibroblasts to induce PDPN expression in OSCC cells. In addition, a retrospective investigation of OSCC patients found that IMP-3 and PDPN expression significantly correlated with lymph node metastasis of OSCC patients. Moreover, co-expression of IMP-3 and PDPN were frequently detected both in primary and lymph nodes metastatic OSCC cells using immunohistochemical dual staining. Thus, the IMP-3-PDPN axis may be a sensitive target molecule in anti-invadopodia therapy for the treatment of metastatic cancers. | - |
dc.description.statementOfResponsibility | open | - |
dc.relation.isPartOf | CARCINOGENESIS | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | Functional invadopodia formation through stabilization of the PDPN transcript by IMP-3 and cancer-stromal crosstalk for PDPN expression. | - |
dc.type | Article | - |
dc.contributor.college | Researcher Institutes (부설 연구소) | - |
dc.contributor.department | Oral Cancer Research Institute (구강종양연구소) | - |
dc.contributor.googleauthor | Young Sun Hwang | - |
dc.contributor.googleauthor | Zhang Xianglan | - |
dc.contributor.googleauthor | Kwang-Kyun Park | - |
dc.contributor.googleauthor | Won-Yoon Chung | - |
dc.identifier.doi | 10.1093/carcin/bgs258 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A01429 | - |
dc.contributor.localId | A03489 | - |
dc.contributor.localId | A03676 | - |
dc.contributor.localId | A04472 | - |
dc.relation.journalcode | J00456 | - |
dc.identifier.eissn | 1460-2180 | - |
dc.identifier.url | http://carcin.oxfordjournals.org/content/33/11/2135.long | - |
dc.contributor.alternativeName | Park, Kwang Kyun | - |
dc.contributor.alternativeName | Zhang, Xiang Lan | - |
dc.contributor.alternativeName | Chung, Won Yoon | - |
dc.contributor.alternativeName | Hwang, Young Sun | - |
dc.contributor.affiliatedAuthor | Park, Kwang Kyun | - |
dc.contributor.affiliatedAuthor | Zhang, Xiang Lan | - |
dc.contributor.affiliatedAuthor | Chung, Won Yoon | - |
dc.contributor.affiliatedAuthor | Hwang, Young Sun | - |
dc.citation.volume | 33 | - |
dc.citation.number | 11 | - |
dc.citation.startPage | 2135 | - |
dc.citation.endPage | 2146 | - |
dc.identifier.bibliographicCitation | CARCINOGENESIS, Vol.33(11) : 2135-2146, 2012 | - |
dc.identifier.rimsid | 31962 | - |
dc.type.rims | ART | - |
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