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HDAC3 positively regulates HE4 expression to promote ovarian carcinoma progression.

Authors
  • Lou, Tong1
  • Zhuang, Huiyu2
  • Liu, Chongdong3
  • Zhang, Zhenyu4
  • 1 Department of Obstetrics and Gynecology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China. , (China)
  • 2 Department of Obstetrics and Gynecology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China. Electronic address: [email protected] , (China)
  • 3 Department of Obstetrics and Gynecology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China. Electronic address: [email protected] , (China)
  • 4 Department of Obstetrics and Gynecology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Archives of Biochemistry and Biophysics
Publisher
Elsevier
Publication Date
Oct 30, 2019
Volume
675
Pages
108044–108044
Identifiers
DOI: 10.1016/j.abb.2019.07.009
PMID: 31302139
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

To identify the relationship between Histone deacetylase 3 (HDAC3) and Human epididymis protein 4 (HE4) and to explore the mechanisms underlying their effects on the malignant behaviors of ovarian carcinoma cells. The expression levels of HDAC3 in ovarian carcinoma tissues were identified by immunohistochemistry, Western blot and real-time PCR. A wound healing assay, a Transwell assay and a CCK8 proliferation assay were used to assess the proliferation, invasion and metastatic capacities of ovarian carcinoma cells before and after transfection and HDAC3 protein treatment. HDAC3 and HE4 protein expression level in epithelial ovarian tissues were detected by immunohistochemistry, and the relationship between them was examined. HE4 was identified as an HDAC3-interacting protein. HDAC3 promotes ovarian carcinoma cell proliferation, invasion and migration by increasing the expression of HE4. HE4 and HDAC3 expression levels were significantly higher in malignant epithelial ovarian tissues than they were in benign and normal epithelial ovarian tissues. HDAC3 gene interference downregulated the expression of the PI3K/AKT signaling pathway-associated molecules P-PI3K/PI3K and P-AKT/AKT. HDAC3 expression is higher in ovarian carcinoma and promotes ovarian carcinoma cell proliferation, invasion and migration. HDAC3 and HE4 binding activates the PI3K/AKT signaling pathway, enhances ovarian carcinoma and promotes ovarian carcinoma cell proliferation, invasion and migration. Therefore, inhibiting the relationship between HDAC3 and HE4 may therefore have potential therapeutic value in patients with ovarian carcinoma. Copyright © 2019 Elsevier Inc. All rights reserved.

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