ArticleTranslational cancer research2020
miRNA-26a blocks interleukin-2-mediated migration and proliferation of non-small cell lung cancer cells via vascular cell adhesion molecule-1.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Tumor Suppressor miRNA-based Signatures in Triple Negative Breast Cancer: A Study Based on Big Data Analysis of Gene Expression Omnibus (GEO) Datasets and Its Validation.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Evaluation of the relationship between inflammatory reaction and interleukins in ovine pulmonary adenocarcinomas.Veterinary research forum : an international quarterly journal · 2023Article
- Cell adhesion molecules and immunotherapy in advanced non-small cell lung cancer: Current process and potential application.Frontiers in oncology · 2023Review
- Research Progress on Therapeutic Targeting of Cancer-Associated Fibroblasts to Tackle Treatment-Resistant NSCLC.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Ascites in ovarian cancer: MicroRNA deregulations and their potential roles in ovarian carcinogenesis.Cancer biomarkers : section A of Disease markers · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLiteratures have confirmed role of inflammatory mediators like interleukin-2 (IL-2) in non-small cell lung cancer (NSCLC). microRNA-26a (miR-26a) is involved in variety of signaling pathways and functions as tumor suppressor and regulating the responsible genes at posttranscriptional level. The aim of study was to study the correlation of IL-2 and miR-26a in lung cancer (LC) cells.
methodsFor the study we selected 32 subjects reported for NSCLC and 20 with chronic obstructive pulmonary disease (COPD) as control in the present study. For
resultsWe evidenced that, expression of miR-26a was suppressed, whereas levels of IL-2 and VCAM-1 were increased in NSCLC tissues. IL-2 down-regulated the levels of miR-26a but upregulated the levels of VCAM-1 in H-460 and H-226 cells. miR-26a modulated the expression level of VCAM-1 via binding the 3'-UTR region. We found that miR-26a attenuated the migration and proliferation of H-460 and H-226 cells. IL-2 modulated the levels of miR-26a via activating p65 but not STAT-3.
conclusionsAll together, the finding of our study show that miR-26a blocks IL-2 mediated proliferation and migration of NSCLC via targeting VCAM-1.
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