ArticleFrontiers in oncology2025
Lnc-CNNM3-DT as a protective factor in cervical cancer: regulation of LIAS expression and intracellular copper levels.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- IRF8 Suppresses Hepatocellular Carcinoma Progression Through LIAS-Dependent IFN Production and Cuproptosis Activation.Genes, chromosomes & cancer · 2026Article
- Cuproptosis: a novel therapeutic mechanism in lung cancer.Cancer cell international · 2025Review
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4 authors.
Funding
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Abstract
Background: Cervical cancer (CC) is the fourth leading cause of cancer-related death in women globally.While early screening has reduced mortality, tumor metastasis remains a significant concern, particularly in developing countries. Recent studies have identified cuproptosis, a copper-dependent cell death mechanism, as a potential factor in tumor progression. Long non-coding RNAs (lncRNAs) are key regulators of tumor progression. This study investigates the role of cuproptosis-related lncRNA (CRL) CNNM3-DT in CC, focusing on its impact on LIAS expression, intracellular copper levels, and tumor progression. Methods: We analyzed the expression of lnc-CNNM3-DT and LIAS in clinical samples and CC cell lines using Real-time Polymerase Chain Reaction (RT-qPCR), Western blot, and immunohistochemistry (IHC). Functional assays, including CCK-8, wound healing, transwell invasion, and flow cytometry, were used to evaluate the effects of lnc-CNNM3-DT overexpression on cell proliferation, migration, invasion, and apoptosis. Intracellular copper ion levels were measured, and correlations between lnc-CNNM3-DT, LIAS, and clinicopathological features were analyzed. Results: Lnc-CNNM3-DT expression was significantly higher in paracancerous tissues and normal cervical epithelial cells compared to tumor tissues and CC cell lines. Overexpression of lnc-CNNM3-DT suppressed proliferation, migration, and invasion of HeLa and SiHa cells while enhancing apoptosis. Additionally, lnc-CNNM3-DT overexpression downregulated LIAS expression and decreased intracellular copper ion levels. Correlation analysis indicated that lnc-CNNM3-DT expression was negatively associated with tumor diameter and depth of invasion, while LIAS expression showed no significant correlation with clinicopathological features. Conclusion: Our findings suggest that lnc-CNNM3-DT functions as a protective factor in CC by inhibiting tumor progression through downregulation of LIAS expression and reduction of intracellular copper levels. These results highlight lnc-CNNM3-DT as a potential biomarker and therapeutic target in CC.
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