Overexpression and oncogenic function of HMGA2 in endometrial serous carcinogenesis
Kwon, Jungeun Sarah
AffiliationUniv Arizona, Coll Med, Dept Pathol
Univ Arizona, Dept Mol & Cellular Biol
MetadataShow full item record
PublisherE-CENTURY PUBLISHING CORP
CitationOverexpression and oncogenic function of HMGA2 in endometrial serous carcinogenesis. 2016, 6 (2):249-59 Am J Cancer Res
RightsAJCR Copyright © 2016 Creative Commons Attribution Non-Commercial License
Collection InformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at firstname.lastname@example.org.
AbstractThe high-mobility group A protein 2 (HMGA2) is a non-histone chromatin factor highly expressed in fetal tissue and malignant tumors but rarely detected within normal adult tissues. The clinical implications and biological functions of HMGA2 in endometrial carcinoma are largely unknown. Here we report that HMGA2 expression was barely detected in benign endometrium samples (2 of 28 samples). However, HMGA2 expression increased significantly from precancerous lesion endometrial glandular dysplasia (7 of 17, 41.2%), to serous endometrial intraepithelial carcinoma (5 of 8, 62.5%) and to full blown endometrial serous carcinoma (39 of 59, 66.1%). Functional characterization of HMGA2 revealed that the gene has both tumor growth promotion and metastasis. In addition, HMGA2 induced epithelial-mesenchymal transition (EMT) through modulation vimentin and β-catenin. Furthermore, HMGA2 overexpression started from endometrial serous precancers, non-invasive cancers, as well as in full blown carcinomas in a p53 knockout mouse model we recently established in our laboratory. Our findings suggest that HMGA2 may serve as a useful diagnostic marker in the assessment of endometrial serous cancer and its precursor lesions.
VersionFinal published version
SponsorsThis study was partially supported by awards from National 863 Program (2014AA020605), and The National Natural Science Foundation of China (81472432, 81272857, 81171897).
CollectionsUA Faculty Publications
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