ArticleJournal of thoracic disease2025
Role of miR-26b in regulating non-small cell lung cancer progression via targeting RCN1.
Article in Journal of thoracic disease, 2025. 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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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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4 authors.
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Abstract
Background: Dysregulated microRNAs (miRNAs) play a crucial role in the progression of non-small cell lung cancer (NSCLC) through post-transcriptional gene regulation. Although miR-26b has been implicated in tumor suppression, its epigenetic regulation and functional targets in NSCLC remain poorly understood. DNA methylation is a well-established modulator of miRNA expression; however, the specific role of miR-26b hypermethylation and its interaction with oncogenic pathways, particularly reticulocalbin-1 (RCN1), have not been fully elucidated. This study aims to clarify the miR-26b/RCN1 regulatory axis in NSCLC pathogenesis. By establishing this mechanism, we seek to identify novel therapeutic strategies and improve patient outcomes. Methods: We first quantified the expression levels of miR-26b in NSCLC cells using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and then evaluated its impact on cell proliferation, migration, and invasion using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, and transwell assays. DNA methylation status was assessed by methylation-specific PCR (MSP) and bisulfite sequencing PCR (BSP). Western blotting and luciferase reporter assays were conducted to confirm the direct binding of miR-26b to the RCN1 3'-untranslated region (3'UTR). Additionally, we examined the effects of the miR-26b/RCN1 axis on NSCLC cell behaviors Results: Our findings demonstrated that RCN1 was a direct target of miR-26b, and miR-26b expression was downregulated due to DNA hypermethylation. Luciferase assays confirmed that miR-26b suppressed RCN1 expression by targeting its 3'UTR. Moreover, overexpression of miR-26b significantly inhibited NSCLC cell proliferation, invasion, and migration by targeting RCN1. Conclusions: Our results indicate that miR-26b plays a critical role in NSCLC progression, suggesting its potential as a therapeutic biomarker for NSCLC patients.
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