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Expression of HOXA10 in Endometrial Hyperplasia and Adenocarcinoma and Regulation by Sex Hormones In Vitro
  1. Gang Zhong, MD*,
  2. Yan Wang, MD*, and
  3. Xuemei Liu, MD*
  1. *Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology; and
  2. Department of Gynecology, Hubei Maternal and Child Health Hospital, Wuhan, Hubei, People's Republic of China.
  1. Address correspondence and reprint requests to Gang Zhong, MD, Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, People's Republic of China. E-mail: gzhongwh{at}


Objective: The objective of the study was to determine the expression of HOXA10 in human endometrial tissue in endometrial hyperplasia and carcinomas, and regulation by sex steroids in Ishikawa cells.

Methods: Endometrial tissue was obtained from 133 subjects with normal endometria, endometrial hyperplasia, or endometrial adenocarcinoma. Among 133 specimens, 20 were normal endometria, 19 were simple hyperplasias without atypia, 20 were complex hyperplasias without atypia, 33 were atypical hyperplasias, and 41 were endometrial adenocarcinomas. The expression of HOXA10 was analyzed by immunohistochemistry. Ishikawa cell lines were incubated with 17β estradiol (10−8 mol/L) alone, medroxyprogesterone acetate (10−6 mol/L) alone, or the combination of estrogen and progesterone for 48 hours, respectively. In certain experiments, the antiprogestin antagonist, RU486 (10−5 mol/L), was also added to Ishikawa cells along with estradiol and medroxyprogesterone acetate for 48 hours. The expression of HOXA10 gene was detected by reverse transcriptase-polymerase chain reaction and Western blotting.

Results: HOXA10 was expressed in both normal and neoplastic endometria. No significant difference in HOXA10 expression was found between normal and hyperplastic endometrial tissues. The expression of HOXA10 was decreased in endometrial adenocarcinomas compared with normal endometria. Estrogen alone, progestin alone, or progestin combined with estrogen could significantly increase the expression of HOXA10 gene (P < 0.05). RU486 could inhibit the effect of up-regulation of HOXA10 expression by progestin.

Conclusions: The expression of HOXA10 was deregulated in endometrial carcinomas and up-regulated by sex hormones.

  • Endometrial hyperplasia
  • Adenocarcinoma
  • HOXA10
  • Regulation

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