Article Text

Download PDFPDF
miR-30d Blocked Transforming Growth Factor β1–Induced Epithelial-Mesenchymal Transition by Targeting Snail in Ovarian Cancer Cells
  1. Zhongxue Ye, MD*,
  2. Le Zhao, PhD*,
  3. Jie Li, MD*,
  4. Wei Chen, PhD and
  5. Xu Li, MD, PhD*
  1. * Centers for Translational Medicine and
  2. Laboratory Medicine, the First Affiliated Hospital, Xi’an Jiaotong University College of Medicine, Xi’an, Shaanxi, People’s Republic of China.
  1. Address correspondence and reprint requests to Xu Li, MD, PhD, Center for Translational Medicine, the First Affiliated Hospital, Xi’an Jiaotong University College of Medicine, 277 W. Yanta Rd, Xi’an, Shaanxi 710061, People’s Republic of China. E-mail: lixu56{at}


Objective MicroRNAs (miRs) are essential regulators of gene expression by suppressing translation or causing degradation of target mRNA. Growing evidence sheds light on the crucial roles of miR dysregulation in cancer development and progression. In this study, we focused on the role of miR-30d in transforming growth factor β1 (TGF-β1)–initiated epithelial-mesenchymal transition (EMT) in ovarian cancer cells.

Methods Transforming growth factor β1 (10 ng/mL) was used to initiate EMT in SKOV3 and 3AO cells. The expression of miR-30 family members was determined by quantitative real-time polymerase chain reaction. Messenger RNA and protein levels of E-cadherin, N-cadherin, vimentin, and Snail were detected by quantitative real-time polymerase chain reaction and Western blot, respectively. Cell migration and invasion capacities were evaluated by Transwell chamber assay. Luciferase activity assay was performed to verify the direct inhibition of Snail by miR-30d.

Results MiR-30b, MiR-30c, and MiR-30d were down-regulated during TGF-β1–induced EMT in SKOV3 and 3AO ovarian cancer cells. Restoration of miR-30d by miR-30d mimic reversed TGF-β1–induced EMT phenotypes including the morphological changes, expression pattern of molecular markers (E-cadherin, N-cadherin), and migratory and invasive capabilities in ovarian cancer cells. Furthermore, Snail was identified as the direct target of miR-30d.

Conclusions Our results revealed that miR-30d functioned as a suppressor of ovarian cancer progression by decreasing Snail expression and thus blocking TGF-β1–induced EMT process, suggesting the potentiality of miR-30d analogs to be used as therapeutics for ovarian cancer.

  • Epithelial-mesenchymal transition
  • miR-30d
  • Ovarian cancer
  • TGF-β1

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.


  • Z.Y and L.Z. contributed equally to this work.

  • This study was supported by the National Natural Science Foundation of China (no. 30973429).

  • The authors declare no conflicts of interest.