ArticleCancer biology & therapy2015
Low miR-145 silenced by DNA methylation promotes NSCLC cell proliferation, migration and invasion by targeting mucin 1.
Article in Cancer biology & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed, 29 citations in OpenAlex.
- MiracleNet: A Biologically Interpretable Machine Learning Model for Resected Non-small-cell Lung Cancer.Computational and structural biotechnology journal · 2026Article
- Diagnostic Potential of Exosomal and Non-Exosomal Biomarkers in Lung Cancer: A Comparative Analysis Using a Rat Model of Lung Carcinogenesis.Non-coding RNA · 2025Article
- Targeting NSCLC drug resistance: Systems biology insights into the MALAT1/miR-145-5p axis and Wip1 in regulating ferroptosis and apoptosis.Journal of the Royal Society, Interface · 2025Article
- Extracellular circulating miRNAs as potential non-invasive biomarkers in non-small cell lung cancer patients.Frontiers in oncology · 2023Review
- Ascites in ovarian cancer: MicroRNA deregulations and their potential roles in ovarian carcinogenesis.Cancer biomarkers : section A of Disease markers · 2022Review
- Diagnostic and prognostic value of serum miR-145 and vascular endothelial growth factor in non-small cell lung cancer.Oncology letters · 2022Article
- LncRNA SENCR promotes cell proliferation and progression in non-small-cell lung cancer cells via sponging miR-1-3p.Cell cycle (Georgetown, Tex.) · 2021Article
- The Risks of miRNA Therapeutics: In a Drug Target Perspective.Drug design, development and therapy · 2021Review
- MiR-145: a potential biomarker of cancer migration and invasion.American journal of translational research · 2019Review
- Epigenetic mechanism and target therapy of UHRF1 protein complex in malignancies.OncoTargets and therapy · 2019Review
- Exploration of bladder cancer-associated methylated miRNAs by methylated DNA immunoprecipitation sequencing.OncoTargets and therapy · 2019Article
- Increased MALAT1 expression contributes to cisplatin resistance in non-small cell lung cancer.Oncology letters · 2018Article
- The role of plasma miRNAs in the diagnosis of pulmonary nodules.Journal of thoracic disease · 2018Article
- Epigenetics and MicroRNAs in Cancer.International journal of molecular sciences · 2018Review
- miR-431-5p alters the epithelial-to-mesenchymal transition markers by targetingOncoTargets and therapy · 2018Article
- miR-145-5p inhibits epithelial-mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non-small cell lung cancer cells.Oncology letters · 2017Article
- Deregulation of miRNAs in malignant pleural mesothelioma is associated with prognosis and suggests an alteration of cell metabolism.Scientific reports · 2017Article
- Placental Homing Peptide-microRNA Inhibitor Conjugates for Targeted Enhancement of Intrinsic Placental Growth Signaling.Theranostics · 2017Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MiR-145 has been implicated in the progression of non-small cell lung cancer (NSCLC); however, its exact mechanism is not well established. Here, we report that miR-145 expression is decreased in NSCLC cell lines and tumor tissues and that this low level of expression is associated with DNA methylation. MiR-145 methylation in NSCLC was correlated with a more aggressive tumor phenotype and was associated with poor survival time, as shown by Kaplan-Meier analysis. Additional multivariate Cox regression analysis indicated that miR-145 methylation was an independent prognostic factor for poor survival in patients with NSCLC. Furthermore, we found that restoration of miR-145 expression inhibited proliferation, migration and invasion of NSCLC by the direct targeting of mucin 1 by miR-145. Our results indicate that low miR-145 expression, due to methylation, promotes NSCLC cell proliferation, migration and invasion by targeting mucin 1. Therefore, miR-145 may be a valuable therapeutic target for NSCLC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.