Volume 43 Issue 2
Mar.  2022
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Suxian ZHANG, Limei FENG, Lu WU, Shaoyan YANG, Qinghua ZHAO. miR-145 Regulates the Expression of OCT4 in Human Endometrial Stromal Cells and Promotes the Development of Endometriosis[J]. Journal of Kunming Medical University, 2022, 43(2): 23-33. doi: 10.12259/j.issn.2095-610X.S20220220
Citation: Suxian ZHANG, Limei FENG, Lu WU, Shaoyan YANG, Qinghua ZHAO. miR-145 Regulates the Expression of OCT4 in Human Endometrial Stromal Cells and Promotes the Development of Endometriosis[J]. Journal of Kunming Medical University, 2022, 43(2): 23-33. doi: 10.12259/j.issn.2095-610X.S20220220

miR-145 Regulates the Expression of OCT4 in Human Endometrial Stromal Cells and Promotes the Development of Endometriosis

doi: 10.12259/j.issn.2095-610X.S20220220
  • Received Date: 2021-12-07
    Available Online: 2022-03-04
  • Publish Date: 2022-03-04
  •   Objective  To further explore the regulatory mechanism of miR-145 in Endometriosis (EMs) through cell experiments.  Methods  miR-145 or octamer-binding transcription factor 4 (OCT4)gene and protein expression levels in cells were examined using reverse transcription-quantitative PCR and western blotting, respectively. Correlation analyses and dualluciferase reporter assays were performed to assess the association between miR-145 and OCT4. A Cell Counting Kit-8 assay was performed to test cell viability, while cell apoptosis was measured using flow cytometry. Moreover, the migration of hESCs was measured via Transwell assays.   Results  In cell assays, overexpression of miR-145 signifcantly promoted proliferation and migration (P < 0.01), but inhibited the apoptosis of hESCs (P < 0.05). Furthermore, the transfection of hESCs with miR-145 mimics decreased the protein expression levels of OCT4, Bax and MMP1 (P < 0.01), as well as increased the protein expression of Bcl-2. However, knockdown of miR-145 reversed these results and significantly inhibited the proliferation of hESCs by targeting OCT4 (P < 0.05).   Conclusion  The present results suggested that knockdown of miR-145 signifcantly suppressed the development of EMs by targeting OCT4, which may serve as a potential target for the treatment of EMs.
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