Overexpression and oncogenic function of HMGA2 in endometrial serous carcinogenesis

Linxuan Wei, Xiaolin Liu, Wenjing Zhang, Yuyan Wei, Yingwei Li, Qing Zhang, Ruifen Dong, Jungeun Sarah Kwon, Zhaojian Liu, Wenxin - Zheng, Beihua Kong

Research output: Contribution to journalArticle

10 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)249-259
Number of pages11
JournalAmerican Journal of Cancer Research
Volume6
Issue number2
StatePublished - 2016

Keywords

  • EMT
  • Endometrial serous carcinoma
  • HMGA2
  • Metastasis
  • Tumor growth

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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  • Cite this

    Wei, L., Liu, X., Zhang, W., Wei, Y., Li, Y., Zhang, Q., Dong, R., Kwon, J. S., Liu, Z., Zheng, W. ., & Kong, B. (2016). Overexpression and oncogenic function of HMGA2 in endometrial serous carcinogenesis. American Journal of Cancer Research, 6(2), 249-259.