The dual roles of circRNAs in Wnt/β-Catenin signaling and cancer progression.

Pathol Res Pract

Department of Pharmacology, College of Pharmacy, King Khalid University, Abha 61421, Aseer, Saudi Arabia.

Published: March 2024

Cancer, a complex pathophysiological condition, arises from the abnormal proliferation and survival of cells due to genetic mutations. Dysregulation of cell cycle control, apoptosis, and genomic stability contribute to uncontrolled growth and metastasis. Tumor heterogeneity, microenvironmental influences, and immune evasion further complicate cancer dynamics. The intricate interplay between circular RNAs (circRNAs) and the Wnt/β-Catenin signalling pathway has emerged as a pivotal axis in the landscape of cancer biology. The Wnt/β-Catenin pathway, a critical regulator of cell fate and proliferation, is frequently dysregulated in various cancers. CircRNAs, a class of non-coding RNAs with closed-loop structures, have garnered increasing attention for their diverse regulatory functions. This review systematically explores the intricate crosstalk between circRNAs and the Wnt/β-Catenin pathway, shedding light on their collective impact on cancer initiation and progression. The review explores the diverse mechanisms through which circRNAs modulate the Wnt/β-Catenin pathway, including sponging microRNAs, interacting with RNA-binding proteins, and influencing the expression of key components in the pathway. Furthermore, the review highlights specific circRNAs implicated in various cancer types, elucidating their roles as either oncogenic or tumour-suppressive players in the context of Wnt/β-Catenin signaling. The intricate regulatory networks formed by circRNAs in conjunction with the Wnt/β-Catenin pathway are discussed, providing insights into potential therapeutic targets and diagnostic biomarkers. This comprehensive review delves into the multifaceted roles of circRNAs in orchestrating tumorigenesis through their regulatory influence on the Wnt/β-Catenin pathway.

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http://dx.doi.org/10.1016/j.prp.2024.155132DOI Listing

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