ArticleCancer management and research2026
CircCDK6 Regulates Stemness Maintenance and Cisplatin Resistance in Lung Adenocarcinoma via the Wnt/β-Catenin Signaling Pathway.
Article in Cancer management and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: This study investigates the role of circCDK6 in maintaining cancer stem cell (CSC) properties and mediating cisplatin resistance in lung adenocarcinoma (LUAD), with a focus on the involvement of the Wnt/β-catenin signaling pathway. Methods: The expression levels of circCDK6 in various LUAD cell lines were measured using quantitative real-time PCR. Gain- and loss-of-function experiments were conducted by plasmid-mediated overexpression and siRNA-mediated knockdown of circCDK6. Cisplatin sensitivity was assessed using the Cell Counting Kit-8 assay and colony formation assay. The involvement of the Wnt/β-catenin pathway was examined by inhibiting the pathway with IWR-1. A subcutaneous xenograft model in BALB/c nude mice was used to evaluate the in vivo effects of circCDK6 knockdown on cisplatin responsiveness, and tumor tissues were analyzed through hematoxylin and eosin staining and immunohistochemistry for Ki-67 expression. Results: CircCDK6 expression was significantly elevated in H1299 and H1975 cells compared to A549 and PC-9 cells. Overexpression of circCDK6 increased stemness markers, such as CD133, Oct4, and Sox2, and enhanced cisplatin resistance, as demonstrated by higher IC Conclusion: CircCDK6 may promote CSC properties and contribute to cisplatin resistance in LUAD, potentially through activation of the Wnt/β-catenin pathway. These findings suggest that circCDK6 may represent a potential therapeutic target for overcoming chemoresistance in LUAD, although further studies are needed to validate its role and clinical relevance.
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