Elevated STC‑1 augments the invasiveness of triple‑negative breast cancer cells through activation of the JNK/c‑Jun signaling pathway
DC Field | Value | Language |
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dc.contributor.author | Han, Jeonghun | - |
dc.contributor.author | Jeon, Myeongjin | - |
dc.contributor.author | Shin, Incheol | - |
dc.contributor.author | Kim, Sangmin | - |
dc.date.accessioned | 2021-08-02T16:28:08Z | - |
dc.date.available | 2021-08-02T16:28:08Z | - |
dc.date.created | 2021-05-12 | - |
dc.date.issued | 2016-09 | - |
dc.identifier.issn | 1021-335X | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/22213 | - |
dc.description.abstract | Stanniocalcin-1 (STC-1), a secreted glycoprotein, is highly expressed in a variety of human malignancies. However, the role of STC-1 has not been fully elucidated in breast cancer cells. Here, we investigated whether STC-1 acts as a prognostic factor in triple-negative breast cancer (TNBC) patients, and we explored the cellular mechanism in breast cancer cells. The level of STC-1 expression was directly associated with the relapse-free and overall survival of basal-type breast cancer patients. Breast cancer patients with a high level of STC-1 had poor prognosis. In addition, our results showed that the level of STC-1 expression was markedly higher in TNBC than in non-TNBC cells. Invasiveness of the TNBC cells was also significantly increased in response to recombinant human STC-1 treatment. In contrast, the invaded cell numbers were completely decreased by STC-1 siRNA overexpression in the Hs578T and MDA-MB-231 TNBC cells. Our results showed that the phosphorylation of c-Jun N-terminal protein kinase (JNK) and c-Jun was increased after STC-1 treatment but not the phosphorylation of ERK and p38 MAPKs in the Hs578T and MDA-MB-231 TNBC cells. Furthermore, expression of one invasion-related gene MMP-9, was increased by STC-1 treatment. STC-1-induced MMP-9 expression was suppressed by SP600125 (a JNK inhibitor) in the Hs578T cells. STC-1-induced cell invasiveness was also inhibited by SP600125. Taken together, we demonstrated that aberrant STC-1 expression is associated with poor prognosis and stimulates the invasiveness of TNBC cells through the JNK/c-Jun-dependent signaling pathway. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | SPANDIDOS PUBL LTD | - |
dc.title | Elevated STC‑1 augments the invasiveness of triple‑negative breast cancer cells through activation of the JNK/c‑Jun signaling pathway | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Shin, Incheol | - |
dc.identifier.doi | 10.3892/or.2016.4977 | - |
dc.identifier.scopusid | 2-s2.0-84980332061 | - |
dc.identifier.wosid | 000382446800070 | - |
dc.identifier.bibliographicCitation | ONCOLOGY REPORTS, v.36, no.3, pp.1764 - 1771 | - |
dc.relation.isPartOf | ONCOLOGY REPORTS | - |
dc.citation.title | ONCOLOGY REPORTS | - |
dc.citation.volume | 36 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 1764 | - |
dc.citation.endPage | 1771 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.subject.keywordPlus | STANNIOCALCIN-1 MESSENGER-RNA | - |
dc.subject.keywordPlus | MESENCHYMAL TRANSITION | - |
dc.subject.keywordPlus | CLINICAL-SIGNIFICANCE | - |
dc.subject.keywordPlus | COLORECTAL-CANCER | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | UP-REGULATION | - |
dc.subject.keywordPlus | INVASION | - |
dc.subject.keywordPlus | MIGRATION | - |
dc.subject.keywordPlus | KINASES | - |
dc.subject.keywordPlus | MARKER | - |
dc.subject.keywordAuthor | stanniocalcin-1 | - |
dc.subject.keywordAuthor | prognosis | - |
dc.subject.keywordAuthor | triple-negative breast cancer | - |
dc.subject.keywordAuthor | cell invasion | - |
dc.subject.keywordAuthor | JNK | - |
dc.identifier.url | https://www.spandidos-publications.com/10.3892/or.2016.4977 | - |
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