The role of S100A14 in epithelial ovarian tumors
Metrics: PDF 5118 views | HTML 3270 views | ?
Hanbyoul Cho1,3, Ha-Yeon Shin1, Sunghoon Kim2,3, Jane Seon-Young Kim1, Joon-Yong Chung4, Eun Joo Chung5, Kyung-Hee Chun6, Stephen M. Hewitt4, Jae-Hoon Kim1,3
1 Department of Obstetrics and Gynecology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea
2 Department of Obstetrics and Gynecology, Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea
3 Institute of Women’s Life Medical Science, Yonsei University College of Medicine, Seoul, Republic of Korea
4 Tissue Array Research Program & Applied Molecular Pathology Lab., Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
5 Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
6 Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul, Republic of Korea
Jae-Hoon Kim, , email:
Keywords: Epithelial ovarian cancer; tumor marker; S100A14; shRNA
Received: February 20, 2014 Accepted: May 6, 2014 Published: May 6, 2014
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.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.