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Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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RNLS promotes ovarian cancer growth and inhibits ferroptosis via mediating STAT3

Liang Lin1, Zuolian Xie1, Peilin Zhong1

  • 1Department of Gynecology, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, China.

Frontiers in Oncology
|August 13, 2025
PubMed
Abstract

Insights

Renalase (RNLS) promotes ovarian cancer (OC) growth by activating STAT3 signaling, which suppresses ferroptosis. Targeting the RNLS-STAT3 pathway offers a potential new treatment strategy for ovarian cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Ovarian cancer (OC) is a leading cause of cancer-related death with limited treatment options.
  • The precise role of renalase (RNLS) in OC progression and its involvement in ferroptosis remain largely unknown.
  • Understanding novel molecular mechanisms is crucial for developing effective OC therapies.

Purpose of the Study:

  • To investigate the role of renalase (RNLS) in ovarian cancer (OC) pathogenesis.
  • To elucidate the mechanism by which RNLS influences STAT3 signaling and ferroptosis in OC.
  • To evaluate the therapeutic potential of targeting the RNLS-STAT3 axis in OC.

Main Methods:

  • Quantitative PCR (qPCR) and Western blotting were used to analyze RNLS and STAT3 expression in OC cells.
  • Stable RNLS knockdown and overexpression cell models were generated using lentiviral vectors.
  • Functional assays assessed cell proliferation, migration, invasion, apoptosis, and reactive oxygen species (ROS) levels.
  • Mitochondrial morphology, in vivo tumor growth, and key molecular markers were evaluated.

Main Results:

  • RNLS expression was significantly upregulated in OC cells, correlating with increased STAT3 expression.
  • RNLS knockdown suppressed OC cell proliferation, migration, invasion, and tumor growth, while inducing apoptosis and ROS.
  • RNLS overexpression had opposite effects, promoting OC progression and inhibiting ferroptosis.
  • STAT3 silencing impaired PI3K/AKT signaling and ferroptosis resistance, effects reversed by RNLS overexpression.

Conclusions:

  • RNLS promotes OC progression by activating STAT3-dependent PI3K/AKT signaling, leading to enhanced proliferation, metastasis, and suppressed ferroptosis.
  • The RNLS-STAT3 signaling axis represents a promising therapeutic target for ovarian cancer treatment.
  • Further research into targeting this axis could lead to novel strategies for managing OC.
Keywords:
PI3K/AKTRNLSSTAT3ovarian canceroxidative stress

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