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WISP2 promotes cell proliferation via targeting ERK and YAP in ovarian cancer cells

Zi-Qing Shi1, Zi-Yan Chen1, Yao Han1

  • 1School of Medicine, Jiaxing University, Jiaxing, 314001, China.

Journal of Ovarian Research
|July 27, 2020
PubMed
Abstract

Insights

WISP2 deletion inhibits ovarian cancer cell growth by impacting ERK signaling pathways. This finding offers new insights into ovarian cancer progression and potential therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Wnt-inducible signaling pathway protein 2 (WISP2) is implicated in various tumor developments.
  • The specific role of WISP2 in ovarian cancer pathogenesis is not well understood.

Purpose of the Study:

  • To investigate the functional role of WISP2 in ovarian cancer.
  • To analyze the effects of WISP2 on ovarian cancer cell proliferation and migration in vitro and in vivo.

Main Methods:

  • Immunohistochemistry and western blotting were used to assess WISP2 expression in ovarian cancer tissues and cell lines.
  • WISP2 deletion was performed to evaluate its impact on cell growth, apoptosis, cell cycle, and migration.
  • Key signaling pathway components including ERK, CEBPα, CEBPβ, and YAP were analyzed.

Main Results:

  • WISP2 was found to be highly expressed in ovarian cancer tissues and cell lines compared to normal ovarian tissue.
  • WISP2 deletion significantly inhibited ovarian cancer cell proliferation, clone formation, and migration.
  • WISP2 loss promoted cell apoptosis and altered the cell cycle, primarily through the inhibition of phosphorylated extracellular signal-related kinase (p-ERK)1/2, CEBPα, and CEBPβ, while activating Yes-associated protein (YAP).

Conclusions:

  • WISP2 deletion effectively inhibits ovarian cancer cell proliferation.
  • The inhibitory effect is mediated by the modulation of ERK signaling pathways.
  • WISP2 represents a potential therapeutic target for ovarian cancer treatment.
Keywords:
ApoptosisOvarian cancerProliferationWISP2

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