miR-203 inhibits ovarian tumor metastasis by targeting BIRC5 and attenuating the TGFβ pathway

Baojin Wang1,2,3, Xia Li4,5,6, Guannan Zhao5,6

  • 1The Third Affiliated Hospital, Zhengzhou University, Zhengzhou, China. 307797362@qq.com.

Abstract

Insights

MicroRNA-203 suppresses ovarian cancer metastasis by targeting BIRC5/survivin and inhibiting epithelial-mesenchymal transition (EMT). This study demonstrates miR-203

Area of Science:

  • Molecular biology
  • Oncology
  • Cell biology

Background:

  • MicroRNA-203 (miR-203) acts as a tumor suppressor in ovarian cancer by targeting Snai2 and inhibiting epithelial-mesenchymal transition (EMT).
  • BIRC5, also known as survivin, promotes EMT in ovarian cancer.
  • Previous findings suggest a role for miR-203 in regulating EMT and tumor suppression.

Purpose of the Study:

  • To investigate the hypothesis that miR-203 inhibits ovarian tumor metastasis by targeting BIRC5 and suppressing EMT.
  • To evaluate the therapeutic potential of miR-203 in combination with survivin inhibition.

Main Methods:

  • Overexpression of miR-203 in ovarian cancer cell lines (SKOV3, OVCAR3) using lentiviral vectors.
  • Assessment of cell migration and invasion using transwell assays.
  • In vivo orthotopic mouse model with intrabursal injection of miR-203-expressing SKOV3 cells.
  • Analysis of survivin and EMT marker expression via Western blot and immunostaining.

Main Results:

  • miR-203 overexpression inhibited EMT by targeting BIRC5 in ovarian cancer cells.
  • Combined miR-203 expression and survivin inhibition (YM155) reduced tumor cell migration and invasion.
  • miR-203 attenuated the TGFβ pathway in ovarian cancer cells.
  • In vivo, miR-203 expression suppressed primary ovarian tumor growth and reduced metastasis to peritoneal organs.

Conclusions:

  • miR-203 effectively inhibits ovarian tumor metastasis.
  • The mechanism involves targeting BIRC5/survivin and attenuating the TGFβ pathway.
  • miR-203 holds potential as a therapeutic agent for ovarian cancer metastasis.

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