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Review
. 2025 Jun:270:155944.
doi: 10.1016/j.prp.2025.155944. Epub 2025 Mar 29.

The function of circular RNAs in regulating Wnt/β-catenin signaling: An innovative therapeutic strategy for breast and gynecological cancers

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Review

The function of circular RNAs in regulating Wnt/β-catenin signaling: An innovative therapeutic strategy for breast and gynecological cancers

Samaneh Kahkesh et al. Pathol Res Pract. 2025 Jun.

Abstract

Breast cancer (BC) and gynecological malignancies, including cervical, ovarian, and uterine cancers, are significant global health challenges due to their high prevalence, complex nature, and elevated mortality rates. Dysregulation of the Wnt/β-catenin signaling pathway is a common feature in gynecological malignancies, contributing to cancer cell growth, progression, migration, and metastasis. Recent studies have highlighted the pivotal role of non-coding RNAs (ncRNAs), particularly circular RNAs (circRNAs), in modulating the Wnt/β-catenin signaling pathway. Acting as sponges for microRNAs (miRNAs), circRNAs regulate key oncogenic and tumor-suppressive processes by influencing Wnt-related components. This research explores the role of circRNAs in breast and gynecological malignancies, focusing on their regulatory effects on the Wnt/β-catenin pathway. The findings reveal that circRNAs modulate critical cellular processes such as proliferation, apoptosis, autophagy, and metastasis, with potential implications for therapeutic interventions. Targeting circRNA-mediated dysregulation of Wnt signaling could offer novel strategies for improving diagnostic precision, treatment efficacy, and survival outcomes in breast and gynecological cancers.

Keywords: Breast cancer; Circular RNAs (circRNAs); Gynecological cancers; Therapeutic targets; Wnt/β-catenin signaling pathway.

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Conflict of interest statement

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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