ArticleMolecular medicine reports2018
miR-25 enhances cell migration and invasion in non-small-cell lung cancer cells via ERK signaling pathway by inhibiting KLF4.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Extracellular Vesicles: A New Source of Biomarkers in Pediatric Solid Tumors? A Systematic Review.Frontiers in oncology · 2022Pooled it
- Krüppel-Like Factor 4, a Hub Gate for Cell Crosstalk in Tumor Microenvironment.Cancer medicine · 2026Review
- Regulatory Effects of Coffee/Chlorogenic Acid and Tea/Epigallocatechin-3-Current issues in molecular biology · 2025Review
- miR-25-3p Modulates Tumor Aggressiveness and Ferroptosis Escape in T24 Bladder Cancer Cells In Vitro.Pharmaceuticals (Basel, Switzerland) · 2025Article
- A novel approach in the identification of microRNAs in malignant pleural effusion for lung cancer diagnosis.Oncology reviews · 2025Review
- MACC1 ablation suppresses the dedifferentiation process of non-CSCs in lung cancer through stabilizing KLF4.Cell death discovery · 2024Article
- Enhancement of endothelial function and attenuation of portal vein injury using mesenchymal stem cells carrying miRNA-25-3p.Scientific reports · 2024Article
- MicroRNA‑mediated regulation in lung adenocarcinoma: Signaling pathways and potential therapeutic implications (Review).Oncology reports · 2023Review
- Article
- The deubiquitinase OTUD1 inhibits non-small cell lung cancer progression by deubiquitinating and stabilizing KLF4.Thoracic cancer · 2022Article
- Review
- MicroRNA-25 promotes cell proliferation, migration and invasion in glioma by directly targeting cell adhesion molecule 2.Experimental and therapeutic medicine · 2022Article
- MicroRNAs' role in the environment-related non-communicable diseases and link to multidrug resistance, regulation, or alteration.Environmental science and pollution research international · 2021Review
- Current research advances in microRNA-mediated regulation of Krüppel-like factor 4 in cancer: a narrative review.Annals of translational medicine · 2021Review
- Expression of miRNA-25 in young and old lung adenocarcinoma.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2021Article
- Recent Discoveries on the Involvement of Krüppel-Like Factor 4 in the Most Common Cancer Types.International journal of molecular sciences · 2020Review
- Article
- Hsa_circ_0043265 Suppresses Proliferation, Metastasis, EMT and Promotes Apoptosis in Non-Small Cell Lung Cancer Through miR-25-3p/FOXP2 Pathway.OncoTargets and therapy · 2020Article
- miR-25 promotes invasion of human non-small cell lung cancer via CDH1.Bioengineered · 2019Article
- KLF4 overexpression decreases the viability, invasion and migration of papillary thyroid cancer cells.Experimental and therapeutic medicine · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years, microRNAs (miRNAs/miRs) have gained increasing interest in cancer research. Increasing evidences demonstrated that miRNAs are important for tumor early detection and prognosis. The present study aimed to explore the function of miR‑25 in non‑small‑cell lung cancer (NSCLC) and its underlying mechanisms. The expression levels of miR‑25 and Krüppel-like factor 4 (KLF4) were assessed in 31 pairs of tissue from patients with NSCLC. In addition, the biological roles of miR‑25 in NSCLC were analyzed via a cell wound healing assay, Transwell invasion and migration assays. Target genes of miR‑25 were predicted using TargetScan and verified via a dual luciferase activity assay, western blotting and reverse transcription‑quantitative polymerase chain reaction. The downstream signaling pathway was confirmed by western blot analysis. In the present study, miR‑25 was overexpressed in 31 NSCLC samples compared with in corresponding normal tissues. Overexpression of miR‑25 using miR‑25 mimics markedly promoted NSCLC cell migration and invasion, while inhibition of miR‑25 exerted the opposite effect. KLF4 was suggested to be a novel target gene of miR‑25 in NSCLC cells. Knockdown of KLF4 promoted the migration and invasion of NSCLC cells, whereas rescue of KLF4 expression reduced cell motion ability in miR‑25‑overexpressing NSCLC cells. Furthermore, it was demonstrated that miR‑25 activated the extracellular signal‑regulated kinase (ERK) signaling pathway, which eventually led to increased vimentin, matrix metalloproteinase 11 and N‑cadherin levels, and the downregulation of E‑cadherin expression by inhibiting the expression of KLF4. In conclusion, miR‑25 was demonstrated to activate the ERK signaling pathway by directly targeting KLF4, promoting cell migration and invasion. The findings of the present study indicated that miR‑25 or KLF4 may serve as a therapeutic target for the treatment of NSCLC.
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