Sox9 overexpression in uterine epithelia induces endometrial gland hyperplasia

Gabriel Gonzalez, Shyamin Mehra, Ying Wang, Haruhiko Akiyama, Richard R. Behringer

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

SOX9 is a high mobility group transcription factor that is required in many biological processes, including cartilage differentiation, endoderm progenitor maintenance, hair differentiation, and testis determination. SOX9 has also been linked to colorectal, prostate, and lung cancer. We found that SOX9 is expressed in the epithelium of the adult mouse and human uterus, predominantly marking the uterine glands. To determine if SOX9 plays a role in the development of endometrial cancer we overexpressed Sox9 in the uterine epithelium using a progesterone receptor-Cre mouse model. Sox9 overexpression in the uterine epithelium led to the formation of simple and complex cystic glandular structures in the endometrium of aged-females. Histological analysis revealed that these structures appeared morphologically similar to structures present in patients with endometrial hyperplastic lesions and endometrial polyps that are thought to be precursors of endometrial cancer. The molecular mechanisms that cause the glandular epithelium to become hyperplastic, leading to endometrial cancer are still poorly understood. These findings indicate that chronic overexpression of Sox9 in the uterine epithelium can induce the development of endometrial hyperplastic lesions. Thus, SOX9 expression may be a factor in the formation of endometrial cancer.

Original languageEnglish (US)
Pages (from-to)204-215
Number of pages12
JournalDifferentiation
Volume92
Issue number4
DOIs
StatePublished - Oct 1 2016

Keywords

  • Cancer
  • Endometrium
  • Sox9
  • Transgenic mouse
  • Uterus

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology
  • Cancer Research

MD Anderson CCSG core facilities

  • Research Animal Support Facility

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