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LncRNA CDIPTOSP-induced destabilization of KLF17 promotes ovarian cancer progression through STAU1-mediated mRNA

Ruiqing Tong1,2, Xiangling Yu3, Bingya Xu3

  • 1Center for Reproduction, The First Affiliated Hospital of Soochow University Suzhou 215006, Jiangsu, China.

American Journal of Translational Research
|June 22, 2026
PubMed

Insights

This study reveals that the long non-coding RNA CDIPTOSP promotes ovarian cancer (OC) progression by interacting with STAU1 to destabilize KLF17 mRNA. Targeting this CDIPTOSP/STAU1/KLF17 axis may offer new therapeutic strategies for OC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Ovarian cancer (OC) is a highly lethal gynecologic malignancy with limited effective early detection and targeted therapies.
  • The complex pathogenesis of OC necessitates further research into novel molecular regulators.

Purpose of the Study:

  • To investigate the role of the long non-coding RNA CDIPTOSP in the progression of ovarian cancer.
  • To elucidate the molecular mechanisms underlying CDIPTOSP's function in OC.

Main Methods:

  • Quantitative analysis of CDIPTOSP expression in OC tissues and cell lines.
  • RNA pull-down assay combined with Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS) to identify binding partners.
  • Functional assays including cell proliferation and migration assays following CDIPTOSP knockdown or overexpression.
  • Analysis of KLF17 mRNA stability and its interaction with the CDIPTOSP-STAU1 complex.

Main Results:

  • CDIPTOSP expression was significantly upregulated in OC tissues and cell lines.
  • Knockdown of CDIPTOSP inhibited OC cell proliferation and migration.
  • CDIPTOSP was found to bind to staufen double-stranded RNA binding protein 1 (STAU1).
  • The CDIPTOSP-STAU1 interaction was crucial for the destabilization of KLF17 mRNA.
  • Modulating KLF17 levels could rescue or abolish the effects of CDIPTOSP on OC cell behavior.

Conclusions:

  • The study identifies a novel regulatory axis involving CDIPTOSP, STAU1, and KLF17 in ovarian cancer progression.
  • CDIPTOSP promotes OC progression through the STAU1-mediated destabilization of KLF17 mRNA.
  • This CDIPTOSP/STAU1/KLF17 pathway represents a potential therapeutic target for ovarian cancer.
Keywords:
CDIPTOSPKLF17STAU1ovarian cancer

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