ArticleMolecular medicine reports2019
ΜicroRNA‑421 promotes the progression of non‑small cell lung cancer by targeting HOPX and regulating the Wnt/β‑catenin signaling pathway.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- DNMT3b promotes proliferation and invasion by mediating HOPX DNA methylation in lung cancer.iScience · 2026Article
- Unraveling the molecular-pathological characteristics and cellular complexity of the tumor immune microenvironment in metastatic non-small cell lung cancer.Cell communication and signaling : CCS · 2025Review
- Ketogenic diet does not promote triple-negative and luminal mammary tumor growth and metastasis in experimental mice.Clinical & experimental metastasis · 2024Article
- HOPX is a tumor-suppressive biomarker that corresponds to T cell infiltration in skin cutaneous melanoma.Cancer cell international · 2023Article
- A LGR5 reporter pig model closely resembles human intestine for improved study of stem cells in disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Liquid biopsies based on DNA methylation as biomarkers for the detection and prognosis of lung cancer.Clinical epigenetics · 2022Review
- Review
- HOPXAmerican journal of physiology. Gastrointestinal and liver physiology · 2021Article
- miR-374a-5p inhibits non-small cell lung cancer cell proliferation and migration via targeting NCK1.Experimental and therapeutic medicine · 2021Article
- MiR-421 Aggravates Neurotoxicity and Promotes Cell Death in Parkinson's Disease Models by Directly Targeting MEF2D.Neurochemical research · 2021Article
- MicroRNAs target the Wnt/β‑catenin signaling pathway to regulate epithelial‑mesenchymal transition in cancer (Review).Oncology reports · 2020Review
- MiR-148b suppressed non-small cell lung cancer progression via inhibiting ALCAM through the NF-κB signaling pathway.Thoracic cancer · 2020Article
- ZFAS1 Promotes Cisplatin Resistance via Suppressing miR-421 Expression in Oral Squamous Cell Carcinoma.Cancer management and research · 2020Article
- LncRNA GATA6-AS inhibits cancer cell migration and invasion in gallbladder cancer by downregulating miR-421.OncoTargets and therapy · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) function as key regulators of numerous types of cancers. miRNA (miR)‑421 expression is dysregulated in a variety of tumors; however, its role in non‑small cell lung cancer (NSCLC) remains unclear. In the present study, the role and molecular mechanism of miR‑421 in NSCLC was investigated. In this study, miRNA (miR)‑421 was upregulated in NSCLC tissues and cell lines used the reverse transcriptase quantitative polymerase chain reaction. Ectopic expression of miR‑421 significantly promoted cell proliferation in vitro and tumor growth in vivo by promoting cell cycle progression via CCK-8, colony formation, EdU assay, xenograft model and cell cycle assay. In addition, miR‑421 inhibited NSCLC cell apoptosis by flow cytometry apoptosis assay, as evidenced by anti‑apoptosis gene Bcl‑2 and apoptosis gene cleaved caspase‑3 and cleaved PARP using western blot assay. Furthermore, miR‑421 promoted cell migration and invasion through EMT process using Transwell and western blot assay. It was also demonstrated that miR‑421 can directly target HOPX by the EGFP reporter assay and western blot assay. MiR‑421 overexpression promoted the protein expression levels of β‑catenin, cyclin D1 and c‑myc by western blot assay, which are the downstream genes of Wnt pathway. These data indicated that miR‑421 may act as an oncogene through the effects of HOPX on the Wnt/β‑catenin signaling pathway and may provide insight into the mechanisms underlying carcinogenesis and the identification of potential biomarkers associated with NSCLC.
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