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HMGA2 and high-grade serous ovarian carcinoma

Journal

JOURNAL OF MOLECULAR MEDICINE-JMM
Volume 91, Issue 10, Pages 1155-1165

Publisher

SPRINGER
DOI: 10.1007/s00109-013-1055-8

Keywords

HMGA2; High-grade serous ovarian carcinoma; Tumorigenesis; Gene function

Funding

  1. Dixon Translation Research Fund
  2. Marsha Rivkin Ovarian Cancer Center Fund

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HMGA2, the High Mobility Group A2 gene, plays a very important role in fetal development and carcinogenesis. As an oncofetal gene, it is upregulated in tumors of both epithelial and mesenchymal tissue origin. Chromosomal translocations of HMGA2 are common in mesenchymal tumors, whereas the regulatory mechanisms of HMGA2 in malignant epithelial tumors are much more complex. As an architectural transcription factor, it is involved in multiple biological pathways by targeting different downstream genes in different cancers. HMGA2 is upregulated in both the early and late stages of high-grade serous ovarian carcinoma (HGSOC) and, according to The Cancer Genomic Atlas, is among a signature of genes overexpressed in ovarian cancer. Recent identification of miR-182 as a mediator of BRCA1 and HMGA2 deregulation in ovarian cancer cells may guide us toward a better understanding of the roles of HMGA2 in ovarian carcinogenesis. In this article, we will review recent developments and findings related to HMGA2, including its regulation, oncogenic properties, major functional pathways associated with the tumorigenesis of HGSOC, and its potential role as a biomarker for clinical application.

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