ArticleCancer cell international2017
MicroRNA-338-3p suppresses cell proliferation and induces apoptosis of non-small-cell lung cancer by targeting sphingosine kinase 2.
Article in Cancer cell international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 49 citations in OpenAlex.
- Circulating microRNAs as diagnostic biomarkers and pathogenic mediators in type 2 diabetic retinopathy: a systematic review.Acta diabetologica · 2026Review
- MicroRNAs in lung cancer: their role in tumor progression, biomarkers, diagnostic, prognostic, and therapeutic relevance.Discover oncology · 2025Review
- Signaling pathways and regulatory networks in quail skeletal muscle development: insights from whole transcriptome sequencing.Poultry science · 2024Article
- RPTOR blockade suppresses brain metastases of NSCLC by interfering the ceramide metabolism via hijacking YY1 binding.Journal of experimental & clinical cancer research : CR · 2024Article
- Article
- Sphingolipid Metabolism and Signaling in Lung Cancer: A Potential Therapeutic Target.Journal of oncology · 2022Review
- Circular RNA circ_0010235 sponges miR-338-3p to play oncogenic role in proliferation, migration and invasion of non-small-cell lung cancer cells through modulating KIF2A.Annals of medicine · 2021Article
- Interaction of microRNAs with sphingosine kinases, sphingosine-1 phosphate, and sphingosine-1 phosphate receptors in cancer.Discover oncology · 2021Review
- miRNA expression profiles in liver grafts of HCV and HIV/HCV-infected recipients, 6 months after liver transplantation.Journal of medical virology · 2021Article
- Molecular interactions of miR-338 during tumor progression and metastasis.Cellular & molecular biology letters · 2021Review
- miR-210-3p Promotes Lung Cancer Development and Progression by Modulating USF1 and PCGF3.OncoTargets and therapy · 2021Article
- Ubiquitination Destabilizes Protein Sphingosine Kinase 2 to Regulate Glioma Malignancy.Frontiers in cellular neuroscience · 2021Article
- MiR-338-3p improved lung adenocarcinoma byArchives of medical science : AMS · 2021Article
- USP15 promotes the apoptosis of degenerative nucleus pulposus cells by suppressing the PI3K/AKT signalling pathway.Journal of cellular and molecular medicine · 2020Article
- Inhibition of sphingosine kinase 2 attenuates hypertrophic scar formation via upregulation of Smad7 in human hypertrophic scar fibroblasts.Molecular medicine reports · 2020Article
- PBMC gene expression profiles of female Bangladeshi adults chronically exposed to arsenic-contaminated drinking water.Environmental pollution (Barking, Essex : 1987) · 2020Article
- Circ_0000003 promotes the proliferation and metastasis of non-small cell lung cancer cells via miR-338-3p/insulin receptor substrate 2.Cell cycle (Georgetown, Tex.) · 2019Article
- Prognostic roles of the expression of sphingosine-1-phosphate metabolism enzymes in non-small cell lung cancer.Translational lung cancer research · 2019Article
- miR‑338‑3p inhibits A549 lung cancer cell proliferation and invasion by targeting AKT and β‑catenin signaling pathways.Molecular medicine reports · 2019Article
- The regulation of Neuropilin 1 expression by miR-338-3p promotes non-small cell lung cancer via changes in EGFR signaling.Molecular carcinogenesis · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLung cancer is the major cause of cancer-related death worldwide, and 80% patients of lung cancer are non-small-cell lung cancer (NSCLC) cases. MicroRNAs are important gene regulators with critical roles in diverse biological processes, including tumorigenesis. Studies indicate that sphingosine kinase 2 (SphK2) promotes tumor progression in NSCLC, but how this occurs is unclear. Thus, we explored the effect of miR-338-3p targeting SphK2 on proliferation and apoptosis of NSCLC cells.
methodsExpression of miR-338-3p and SphK2 in NSCLC A549 and H1299 cell lines was measured using qRT-PCR and Western blot. CCK-8 and colony formation assays were used to assess the effect of miR-338-3p on NSCLC cell line proliferation. Flow cytometry was used to study the effect of miR-338-3p on NSCLC apoptosis. Luciferase reporter assay and Western blot were used to confirm targeting of SphK2 by miR-338-3p. Finally, in vivo tumorigenesis studies were used to demonstrate subcutaneous tumor growth.
resultsmiR-338-3p expression in 34 NSCLC clinical samples was downregulated and this was correlated with TNM stage. miR-338-3p significantly suppressed proliferation and induced apoptosis of NSCLC A549 and H1299 cells in vitro. SphK2 was a direct target of miR-338-3p. Overexpression of miR-338-3p significantly inhibited SphK2 expression and reduced luciferase reporter activity containing the SphK2 3'-untranslated region (3'-UTR) through the first binding site. SphK2 lacking 3'-UTR restored the effects of miR-338-3p on cell proliferation inhibition. miR-338-3p significantly inhibited tumorigenicity of NSCLC A549 and H1299 cells in a nude mouse xenograft model.
conclusionsCollectively, miR-338-3p inhibited cell proliferation and induced apoptosis of NSCLC cells by targeting and down-regulating SphK2, and miR-338-3p could inhibit NSCLC cells A549 and H1299 growth in vivo, suggesting a potential mechanism of NSCLC progression. Therapeutically, miR-338-3p may serve as a potential target in the treatment of human lung cancer.
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