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Copyright (c) 2025 Tongwei Xiang, Liping Chen, Huaying Wang, Tao Yu, Tang Li, Jipeng Li, Wanjun Yu
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.CircFOXK2 induces non-small cell lung cancer tumorigenesis through the miR-328-5p/PKP3 axis
Corresponding Author(s) : Tongwei Xiang
Cellular and Molecular Biology,
Vol. 71 No. 11: Issue 11
Abstract
Circular RNAs (circRNAs) are non-coding RNAs (ncRNAs) implicated in the onset and advancement of various human cancers. Among these, circFOXK2 has been linked to non-small cell lung cancer (NSCLC); however, its precise functions and underlying molecular mechanisms are not fully understood. This study shows the first experimental findings that circFOXK2 promotes NSCLC tumor progression by modulating the miR-328-5p/PKP3 signaling pathway. Levels of circFOXK2, miR-328-5p, and PKP3 were evaluated by qRT-PCR. Cellular (NSCLSC) proliferation was examined via CCK-8 assays, migratory capacity via wound healing, and invasive potential via Transwell assays. Potential binding interactions between miR-328-5p and circFOXK2 were first assessed using bioinformatic analysis and verified using a dual-luciferase reporter assay (DLRGAs). Regulatory relationships among circFOXK2, miR-328-5p, and PKP3 were further investigated through qRT-PCR analysis. Elevated expression of circFOXK2 and reduced levels of miR-328-5p were observed in NSCLC cell lines and tissues. Functionally, circFOXK2 enhanced cellular propagation, dissemination, and invasion in vitro. Mechanistic evaluation revealed that circFOXK2 upregulates PKP3 by acting as an miR-328-5p sponge. The findings demonstrate that circFOXK2 contributes to NSCLC tumorigenesis via modulation of the miR-328-5p/PKP3 pathway, identifying this signaling axis as a potential therapeutic target in NSCLC.
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