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International Journal of Molecular Medicine
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2014-January Volume 33 Issue 1

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Downregulation of miR-183 inhibits apoptosis and enhances the invasive potential of endometrial stromal cells in endometriosis

  • Authors:
    • Xiao-Yan Shi
    • Lin Gu
    • Jie Chen
    • Xi-Rong Guo
    • Ying-Li Shi
  • View Affiliations / Copyright

    Affiliations: State Key Laboratory of Reproductive Medicine, Department of Gynecology, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China
    Copyright: © Shi et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].
  • Pages: 59-67
    |
    Published online on: October 25, 2013
       https://doi.org/10.3892/ijmm.2013.1536
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Abstract

Endometriosis is a common gynecological disease, yet its pathogenesis remains poorly understood. Recent studies have demonstrated that the aberrant expression of certain microRNAs (miRNAs) may correlate with the development and progression of endometriosis. In this study, we profiled several differentially expressed miRNAs in the normal, eutopic and ectopic endometrium by miRNA microarray screening analysis, among which, miR-183 was found to be downregulated in the ectopic and eutopic tissues, and the result was further confirmed by real-time PCR (qPCR). Functional analysis indicated that miR-183 plays a promotional role in endometrial stromal cell (ESC) apoptosis and has a negative regulatory impact on the invasive ability of cells, although it has no effect on ESC proliferation. Ovarian steroids (17β-estradiol and progesterone) and inflammatory factors (tumor necrosis factor-α and interleukin-6) decreased the expression of miR-183 in the ESCs. This regulatory function may further manifest the growth and invasive potential of ESCs by altering the expression of miR-183. These findings suggest that the downregulation of miR-183 expression is involved in the development and progression of endometriosis.
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Copy and paste a formatted citation
Spandidos Publications style
Shi X, Gu L, Chen J, Guo X and Shi Y: Downregulation of miR-183 inhibits apoptosis and enhances the invasive potential of endometrial stromal cells in endometriosis. Int J Mol Med 33: 59-67, 2014.
APA
Shi, X., Gu, L., Chen, J., Guo, X., & Shi, Y. (2014). Downregulation of miR-183 inhibits apoptosis and enhances the invasive potential of endometrial stromal cells in endometriosis. International Journal of Molecular Medicine, 33, 59-67. https://doi.org/10.3892/ijmm.2013.1536
MLA
Shi, X., Gu, L., Chen, J., Guo, X., Shi, Y."Downregulation of miR-183 inhibits apoptosis and enhances the invasive potential of endometrial stromal cells in endometriosis". International Journal of Molecular Medicine 33.1 (2014): 59-67.
Chicago
Shi, X., Gu, L., Chen, J., Guo, X., Shi, Y."Downregulation of miR-183 inhibits apoptosis and enhances the invasive potential of endometrial stromal cells in endometriosis". International Journal of Molecular Medicine 33, no. 1 (2014): 59-67. https://doi.org/10.3892/ijmm.2013.1536
Copy and paste a formatted citation
x
Spandidos Publications style
Shi X, Gu L, Chen J, Guo X and Shi Y: Downregulation of miR-183 inhibits apoptosis and enhances the invasive potential of endometrial stromal cells in endometriosis. Int J Mol Med 33: 59-67, 2014.
APA
Shi, X., Gu, L., Chen, J., Guo, X., & Shi, Y. (2014). Downregulation of miR-183 inhibits apoptosis and enhances the invasive potential of endometrial stromal cells in endometriosis. International Journal of Molecular Medicine, 33, 59-67. https://doi.org/10.3892/ijmm.2013.1536
MLA
Shi, X., Gu, L., Chen, J., Guo, X., Shi, Y."Downregulation of miR-183 inhibits apoptosis and enhances the invasive potential of endometrial stromal cells in endometriosis". International Journal of Molecular Medicine 33.1 (2014): 59-67.
Chicago
Shi, X., Gu, L., Chen, J., Guo, X., Shi, Y."Downregulation of miR-183 inhibits apoptosis and enhances the invasive potential of endometrial stromal cells in endometriosis". International Journal of Molecular Medicine 33, no. 1 (2014): 59-67. https://doi.org/10.3892/ijmm.2013.1536
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