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The role of S100A14 in epithelial ovarian tumors

Authors
 Hanbyoul Cho  ;  Ha-Yeon Shin  ;  Sunghoon Kim  ;  Jane Seon-Young Kim  ;  Joon-Yong Chung  ;  Eun Joo Chung  ;  Kyung-Hee Chun  ;  Stephen M. Hewitt  ;  Jae-Hoon Kim 
Citation
 ONCOTARGET , Vol.5(11) : 3482-3496, 2014 
Journal Title
ONCOTARGET
Issue Date
2014
MeSH
Animals ; Biomarkers, Tumor/biosynthesis ; Biomarkers, Tumor/genetics ; Calcium-Binding Proteins/biosynthesis* ; Calcium-Binding Proteins/genetics ; Cell Line, Tumor ; Cell Movement/genetics ; Disease Progression ; Female ; Gene Knockdown Techniques ; Heterografts ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasms, Glandular and Epithelial/genetics ; Neoplasms, Glandular and Epithelial/metabolism* ; Neoplasms, Glandular and Epithelial/pathology ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/metabolism* ; Ovarian Neoplasms/pathology ; Phosphatidylinositol 3-Kinases/metabolism ; Prognosis ; Proto-Oncogene Proteins c-akt/metabolism ; Real-Time Polymerase Chain Reaction ; Survival Analysis
Keywords
Epithelial ovarian cancer ; tumor marker ; S100A14 ; shRNA
Abstract
S100A14 is an EF-hand calcium-binding protein that has been reported to be involved in the progression of many malignancies. However, its role in ovarian cancer has not yet been clarified. In this study, we investigated the significance of S100A14 expression in epithelial ovarian cancers (EOCs) as well as it's mechanism of action. On both RNA and protein levels, S100A14 was overexpressed in transformed cells. Immunohistochemical staining demonstrated that S100A14 expression was associated with advanced stage (P<0.001) and poor tumor grade (P<0.001). Moreover, S100A14 overexpression was an independent prognostic factor for overall survival (HR = 4.53, P = 0.029). We also investigated S100A14's functional role by employing lentiviral-mediated overexpression and knockdown in EOC cells. S100A14 overexpression promoted cell proliferation, tumorigenesis, migration, and invasion, whereas S100A14 knockdown inhibited these properties. TOV112D cells that overexpressed S100A14 also exhibited greater tumor growth potential in xenografted mice. S100A14 promoted such a malignant phenotype in EOC cells through the PI3K/Akt pathway. Taken together, our data indicate that S100A14 has a crucial role in EOC progression, and its overexpression is associated with poor prognosis. Further study of S100A14's molecular mechanisms may lead to the development of a novel therapeutic target for ovarian cancer.
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Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Obstetrics and Gynecology (산부인과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Kim, Seon Young(김선영)
Kim, Sung Hoon(김성훈) ORCID logo https://orcid.org/0000-0002-1645-7473
Kim, Jae Hoon(김재훈) ORCID logo https://orcid.org/0000-0001-6599-7065
Shin, Ha Yeon(신하연)
Chun, Kyung Hee(전경희) ORCID logo https://orcid.org/0000-0002-9867-7321
Cho, Hanbyoul(조한별) ORCID logo https://orcid.org/0000-0002-6177-1648
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/99018
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