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RMI2 knockdown suppresses ovarian cancer cell growth by impairing DNA damage repair via the ATR/CHK1 signaling

Kean Zhu1, Zhao Li1, Yingying Wei1

  • 1Department of Gynecology, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), Changsha, 410000, Hunan, China.

In Vitro Cellular & Developmental Biology. Animal
|July 10, 2026
PubMed

Insights

RecQ-mediated genome instability protein 2 (RMI2) promotes ovarian cancer (OC) by activating the ATR/CHK1 pathway. Inhibiting RMI2 enhances DNA damage and apoptosis, suggesting RMI2 as a therapeutic target for OC.

Area of Science:

  • Genomic instability
  • DNA repair pathways
  • Ovarian cancer biology

Background:

  • RecQ-mediated genome instability protein 2 (RMI2) is upregulated in cancers, but its role in ovarian cancer (OC) is unknown.
  • RMI2 is a component of the RecQ helicase complex involved in genome maintenance.

Purpose of the Study:

  • To investigate the role of RMI2 in ovarian cancer (OC) progression.
  • To determine if RMI2 contributes to OC via the ATR/CHK1 pathway.

Main Methods:

  • Bioinformatics analysis and experimental validation of RMI2 expression in OC tissues and cell lines.
  • Functional assays including RMI2 knockdown, cell proliferation, colony formation, apoptosis, and DNA damage assessment (γH2AX).
  • Investigation of RMI2 interaction with ATR and its effect on the ATR/CHK1 pathway, including experiments with Olaparib and ATR overexpression.

Main Results:

  • RMI2 is highly expressed in OC tissues and cell lines.
  • RMI2 knockdown inhibited OC cell proliferation, colony formation, induced G2/M arrest, and promoted apoptosis.
  • RMI2 knockdown increased DNA damage, downregulated homologous recombination repair proteins, and synergistically enhanced apoptosis under Olaparib treatment.
  • RMI2 directly interacted with ATR, and its knockdown reduced ATR phosphorylation and CHK1 expression. ATR overexpression partially rescued RMI2 knockdown effects.

Conclusions:

  • RMI2 promotes OC development by activating the ATR/CHK1 pathway to maintain genomic stability.
  • RMI2 is a potential prognostic biomarker and therapeutic target for ovarian cancer.
Keywords:
ATR/CHK1 signaling pathwayDNA damage repairOvarian cancerRMI2

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