Overexpression and oncogenic function of HMGA2 in endometrial serous carcinogenesis

Persistent Link:
http://hdl.handle.net/10150/614759
Title:
Overexpression and oncogenic function of HMGA2 in endometrial serous carcinogenesis
Author:
Wei, Linxuan; Liu, Xiaolin; Zhang, Wenjing; Wei, Yuyan; Li, Yingwei; Zhang, Qing; Dong, Ruifen; Kwon, Jungeun Sarah; Liu, Zhaojian; Zheng, Wenxin; Kong, Beihua
Affiliation:
Univ Arizona, Coll Med, Dept Pathol; Univ Arizona, Dept Mol & Cellular Biol
Issue Date:
2016
Publisher:
E-CENTURY PUBLISHING CORP
Citation:
Overexpression and oncogenic function of HMGA2 in endometrial serous carcinogenesis. 2016, 6 (2):249-59 Am J Cancer Res
Journal:
American journal of cancer research
Rights:
AJCR Copyright © 2016 Creative Commons Attribution Non-Commercial License
Collection Information:
This 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 repository@u.library.arizona.edu.
Abstract:
The 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.
ISSN:
2156-6976
PubMed ID:
27186400
Keywords:
HMGA2; endometrial serous carcinoma; tumor growth; metastasis; EMT
Version:
Final published version
Sponsors:
This study was partially supported by awards from National 863 Program (2014AA020605), and The National Natural Science Foundation of China (81472432, 81272857, 81171897).
Additional Links:
http://www.ajcr.us/files/ajcr0023677.pdf

Full metadata record

DC FieldValue Language
dc.contributor.authorWei, Linxuanen
dc.contributor.authorLiu, Xiaolinen
dc.contributor.authorZhang, Wenjingen
dc.contributor.authorWei, Yuyanen
dc.contributor.authorLi, Yingweien
dc.contributor.authorZhang, Qingen
dc.contributor.authorDong, Ruifenen
dc.contributor.authorKwon, Jungeun Sarahen
dc.contributor.authorLiu, Zhaojianen
dc.contributor.authorZheng, Wenxinen
dc.contributor.authorKong, Beihuaen
dc.date.accessioned2016-06-24T23:17:01Z-
dc.date.available2016-06-24T23:17:01Z-
dc.date.issued2016-
dc.identifier.citationOverexpression and oncogenic function of HMGA2 in endometrial serous carcinogenesis. 2016, 6 (2):249-59 Am J Cancer Resen
dc.identifier.issn2156-6976-
dc.identifier.pmid27186400-
dc.identifier.urihttp://hdl.handle.net/10150/614759-
dc.description.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.en
dc.description.sponsorshipThis study was partially supported by awards from National 863 Program (2014AA020605), and The National Natural Science Foundation of China (81472432, 81272857, 81171897).en
dc.language.isoenen
dc.publisherE-CENTURY PUBLISHING CORPen
dc.relation.urlhttp://www.ajcr.us/files/ajcr0023677.pdfen
dc.rightsAJCR Copyright © 2016 Creative Commons Attribution Non-Commercial Licenseen
dc.subjectHMGA2en
dc.subjectendometrial serous carcinomaen
dc.subjecttumor growthen
dc.subjectmetastasisen
dc.subjectEMTen
dc.titleOverexpression and oncogenic function of HMGA2 in endometrial serous carcinogenesisen
dc.typeArticleen
dc.contributor.departmentUniv Arizona, Coll Med, Dept Patholen
dc.contributor.departmentUniv Arizona, Dept Mol & Cellular Biolen
dc.identifier.journalAmerican journal of cancer researchen
dc.description.collectioninformationThis 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 repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen

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