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Article

Estrogen and estrogen receptor induce matrix metalloproteinase-26 expression in endometrial carcinoma cells

  • Authors:
    • Hirotaka Nishi
    • Masahiko Kuroda
    • Keiichi Isaka
  • View Affiliations / Copyright

    Affiliations: Department of Obstetrics and Gynecology, Tokyo Medical University, Shinjuku-ku, Tokyo 160-0023, Japan, Department of Molecular Pathology, Tokyo Medical University, Shinjuku-ku, Tokyo 160-0023, Japan
  • Pages: 751-756
    |
    Published online on: June 7, 2013
       https://doi.org/10.3892/or.2013.2527
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Abstract

The human matrix metalloproteinase (MMP)-26, also called matrilysin-2 or endometase, has been isolated as a matrilysin (MMP-7) homolog. Several reports describe that MMP-26 may be related to the development of endometrial carcinomas. Total RNAs were isolated from 51 normal endometrial tissue samples, 6 endometrial hyperplasia tissue samples and 30 endometrial carcinomas. Real-time reverse transcription-polymerase chain reaction (RT-PCR) was performed to evaluate MMP-26 mRNA expression levels. We examined the effect of estrogen and its receptor (ER) on MMP-26 expression in endometrial carcinoma cell lines by real-time RT-PCR, western blot analysis and luciferase assays. To examine protein-DNA binding between ER and MMP-26 promoter, we performed chromatin immunoprecipitation (ChIP) assay. Real-time RT-PCR analysis revealed that MMP-26 mRNA expression was significantly higher in the normal human endometria and hyperplasias compared with that in endometrial carcinomas. Estrogen not only transactivated the MMP-26 promoter activity but also enhanced endogenous MMP-26 expression. The MMP-26 promoter region contains a putative ER response element (ERE). Nuclear ER protein interacted with ERE on the MMP-26 promoter by ChIP assay. We found a significant difference in MMP-26 expression in normal and malignant endometrial tissue samples and that estrogen induced MMP-26 expression. Estrogen may induce endometrial hyperplasia but not endometrial carcinoma. Our results provide evidence that regulation of MMP-26 promoter activity by estrogen may represent a mechanism for endometrial carcinogenesis.
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Copy and paste a formatted citation
Spandidos Publications style
Nishi H, Kuroda M and Isaka K: Estrogen and estrogen receptor induce matrix metalloproteinase-26 expression in endometrial carcinoma cells. Oncol Rep 30: 751-756, 2013.
APA
Nishi, H., Kuroda, M., & Isaka, K. (2013). Estrogen and estrogen receptor induce matrix metalloproteinase-26 expression in endometrial carcinoma cells. Oncology Reports, 30, 751-756. https://doi.org/10.3892/or.2013.2527
MLA
Nishi, H., Kuroda, M., Isaka, K."Estrogen and estrogen receptor induce matrix metalloproteinase-26 expression in endometrial carcinoma cells". Oncology Reports 30.2 (2013): 751-756.
Chicago
Nishi, H., Kuroda, M., Isaka, K."Estrogen and estrogen receptor induce matrix metalloproteinase-26 expression in endometrial carcinoma cells". Oncology Reports 30, no. 2 (2013): 751-756. https://doi.org/10.3892/or.2013.2527
Copy and paste a formatted citation
x
Spandidos Publications style
Nishi H, Kuroda M and Isaka K: Estrogen and estrogen receptor induce matrix metalloproteinase-26 expression in endometrial carcinoma cells. Oncol Rep 30: 751-756, 2013.
APA
Nishi, H., Kuroda, M., & Isaka, K. (2013). Estrogen and estrogen receptor induce matrix metalloproteinase-26 expression in endometrial carcinoma cells. Oncology Reports, 30, 751-756. https://doi.org/10.3892/or.2013.2527
MLA
Nishi, H., Kuroda, M., Isaka, K."Estrogen and estrogen receptor induce matrix metalloproteinase-26 expression in endometrial carcinoma cells". Oncology Reports 30.2 (2013): 751-756.
Chicago
Nishi, H., Kuroda, M., Isaka, K."Estrogen and estrogen receptor induce matrix metalloproteinase-26 expression in endometrial carcinoma cells". Oncology Reports 30, no. 2 (2013): 751-756. https://doi.org/10.3892/or.2013.2527
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