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Cellular inhibitor of apoptosis protein 2 promotes the epithelial-mesenchymal transition in triple-negative breast cancer cells through activation of the AKT signaling pathway

Authors
 Su Ji Jo  ;  Pil-Gu Park  ;  Hye-Ran Cha  ;  Sung Gwe Ahn  ;  Min Jung Kim  ;  Hyemi Kim  ;  Ja Seung Koo  ;  Joon Jeong  ;  Jeon Han Park  ;  Seung Myung Dong  ;  Jae Myun Lee 
Citation
 Oncotarget, Vol.8(45) : 78781-78795, 2017 
Journal Title
 Oncotarget 
Issue Date
2017
Keywords
AKT signaling pathway ; cellular inhibitor of apoptosis protein 2 ; epithelial-mesenchymal transition ; triple-negative breast cancer
Abstract
Triple-negative breast cancer (TNBC) represents approximately 10-17% of all breast cancers, and patients with TNBC show a poorer short-term prognosis than patients with other types of breast cancer. TNBCs also have a higher tendency for early distant metastasis and cancer recurrence due to induction of the epithelial-mesenchymal transition (EMT). Several recent reports have suggested that inhibitor of apoptosis (IAP) proteins function as regulators of the EMT. However, the roles of these proteins in TNBC are not clear. Accordingly, we investigated the roles of cIAP2 in TNBC. Among eight IAP genes, only cIAP2 was upregulated in TNBC cells compared with that in other breast cancer subtypes. Analysis of TMAs revealed that expression of cIAP2 was upregulated in TNBCs. In vitro studies showed that cIAP2 was highly expressed in TNBC cells compared with that in other types of breast cancer cells. Furthermore, silencing of cIAP2 in TNBC cells induced mesenchymal-epithelial transition (MET)-like processes and subsequently suppressed the migratory ability and invasion capacity of the cells by regulation of Snail through the AKT signaling pathway. In contrast, ectopic expression of cIAP2 in luminal-type breast cancer cells induced activation of the AKT signaling pathway. These results collectively indicated that cIAP2 regulated the EMT in TNBC via activation of the AKT signaling pathway, contributing to metastasis in TNBC. Our study proposes a novel mechanism through which cIAP2 regulates the EMT involving AKT signaling in TNBC cells. We suggest that cIAP2 may be an attractive candidate molecule for the development of targeted therapeutics in the future
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DOI
10.18632/oncotarget.20227
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers
Yonsei Authors
구자승(Koo, Ja Seung) ORCID logo https://orcid.org/0000-0003-4546-4709
박전한(Park, Jeon Han) ORCID logo https://orcid.org/0000-0001-9604-3205
박필구(Park, Pil Gu) ORCID logo https://orcid.org/0000-0002-3024-3439
안성귀(Ahn, Sung Gwe) ORCID logo https://orcid.org/0000-0002-8778-9686
이재면(Lee, Jae Myun) ORCID logo https://orcid.org/0000-0002-5273-3113
정준(Jeong, Joon) ORCID logo https://orcid.org/0000-0003-0397-0005
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URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/161235
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