ArticleFrontiers in oncology2025
RNLS promotes ovarian cancer growth and inhibits ferroptosis via mediating STAT3.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Renalase knockdown inhibits proliferation of mouse satellite cells.Molecular biology reports · 2026Article
- Advances in ferroptosis research in ovarian cancer: molecular mechanisms and therapeutic perspectives.American journal of cancer research · 2026Review
- Advancing the frontiers of ovarian cancer therapy: a comprehensive synthesis of emerging cell death paradigms.Oncology reviews · 2026Review
- LncRNA-PRLB drives ovarian cancer progression and chemoresistance by stabilizing GPX4 mRNA through the FUS-mediated suppression of ferroptosis.Frontiers in medicine · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Ovarian cancer (OC) is a lethal malignancy for which there are limited therapeutic options. The role of renalase (RNLS) in cancer progression and ferroptosis regulation remains unclear. This study investigates how RNLS mediates STAT3 to promote OC growth and suppress ferroptosis. Methods: RNLS expression was analyzed in OC cell lines (OVCAR3) and normal ovarian epithelial cells (IOSE80) via qPCR. Stable RNLS knockdown (sh-RNLS) and overexpression (ov-RNLS) OVCAR3 models were established via lentiviral infection. STAT3 siRNA was transfected to explore RNLS-STAT3 interactions. Functional assays (CCK8, wound healing, Transwell, flow cytometry) evaluated proliferation, migration, invasion, apoptosis, and ROS levels. Mitochondrial morphology was assessed by electron microscopy. Subcutaneous tumor models in mice validated Results: RNLS was significantly upregulated in OC cells, particularly OVCAR3. RNLS knockdown suppressed STAT3 expression, cell proliferation, migration, invasion, and tumor growth, while promoting apoptosis, ROS accumulation, and mitochondrial damage. Conversely, RNLS overexpression exerted opposing effects. STAT3 silencing inhibited PI3K/AKT signaling and ferroptosis resistance, which were rescued by RNLS overexpression. Conclusion: RNLS drives OC progression by activating STAT3-dependent PI3K/AKT signaling, enhancing proliferation, metastasis, and ferroptosis suppression. Targeting RNLS-STAT3 axis may offer a novel therapeutic strategy against OC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.