ArticleFrontiers in pharmacology2018
MiR-3188 Inhibits Non-small Cell Lung Cancer Cell Proliferation Through FOXO1-Mediated mTOR-p-PI3K/AKT-c-JUN Signaling Pathway.
Article in Frontiers in pharmacology, 2018. 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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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- The lncRNA, CyKILRb acts as a ceRNA for tumor suppressive microRNA to augment oncogenic phenotype via induction of PIK3R2/PIMolecular therapy. Nucleic acids · 2026Article
- FOXO1 in cancer: context-dependent roles, microRNA regulation, and therapeutic opportunities.Discover oncology · 2026Review
- Non-coding RNAs and regulation of the PI3K signaling pathway in lung cancer: Recent insights and potential clinical applications.Non-coding RNA research · 2025Review
- miR-486-5p diagnosed atrial fibrillation, predicted the risk of left atrial fibrosis, and regulated angiotensin II-induced cardiac fibrosis via modulating PI3K/Akt signaling through targeting FOXO1.Molecular and cellular biochemistry · 2025Article
- Fibroblast PI3K/AKT signaling and extracellular matrix homeostasis: mechanisms, targets, and delivery challenges.Frontiers in cell and developmental biology · 2025Review
- Article
- miR-3188 inhibits hepatitis B virus transcription by targeting Bcl-2.Archives of virology · 2024Article
- Modulating Effects of Cancer-Derived Exosomal miRNAs and Exosomal Processing by Natural Products.Cancers · 2023Review
- The small molecule chemical compound cinobufotalin attenuates resistance to DDP by inducing ENKUR expression to suppress MYH9-mediated c-Myc deubiquitination in lung adenocarcinoma.Acta pharmacologica Sinica · 2022Article
- Small biomarkers with massive impacts: PI3K/AKT/mTOR signalling and microRNA crosstalk regulate nasopharyngeal carcinoma.Biomarker research · 2022Review
- Circ_0017639 facilitates proliferative, migratory, and invasive potential of non-small cell lung cancer (NSCLC) cells via PI3K/AKT signaling pathway.Bioengineered · 2022Article
- Uncovering the Anti-Lung-Cancer Mechanisms of the Herbal Drug FDY2004 by Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- MicroRNA-147 targets BDNF to inhibit cell proliferation, migration and invasion in non-small cell lung cancer.Oncology letters · 2020Article
- The lncRNA NORAD/miR-520a-3p Facilitates Malignancy in Non-Small Cell Lung Cancer via PI3k/Akt/mTOR Signaling Pathway.OncoTargets and therapy · 2020Article
- Up-regulation of circ_0000353 impedes the proliferation and metastasis of non-small cell lung cancer cells via adsorbing miR-411-5p and increasing forkhead box O1.Cancer biomarkers : section A of Disease markers · 2020Article
- Potential Impact of MicroRNA Gene Polymorphisms in the Pathogenesis of Diabetes and Atherosclerotic Cardiovascular Disease.Journal of personalized medicine · 2019Review
- Article
- miR-1271 enhances the sensitivity of colorectal cancer cells to cisplatin.Experimental and therapeutic medicine · 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
This study investigated the role of miR-3188 on the proliferation of non-small cell lung cancer cells and its relationship to FOXO1-modulated feedback loop. Two non-small cell lung cancer (NSCLC) cell lines A549 and H1299 were used. RNA silencing was achieved by lentiviral transfection. Cell proliferation was assessed by immunohistochemical staining of Ki67 and PCNA, Edu incorporation, and colony formation assay. Western blotting was used to examine expression of FOXO1, mTOR, p-mTOR, CCND1, p21, c-JUN, AKT, pAKT, PI3K, p-PI3K, and p27 proteins. It was found that miR-3188 reduced cell proliferation in NSCLC cells. Molecular analyses indicated that the effect of mammalian target of rapamycin (mTOR) was directly mediated by miR-3188, leading to p-PI3K/p-AKT/c-JUN inactivation. The inhibition of this signaling pathway further caused cell-cycle suppression. Moreover, FOXO1 was found to be involved in regulating the interaction of miR-3188 and mTOR through p-PI3K/p-AKT/c-JUN signaling pathway. Taken together, our study demonstrated that miR-3188 interacts with mTOR and FOXO1 to inhibit NSCLC cell proliferation through a mTOR-p-PI3K/AKT-c-JUN signaling pathway. Therefore, miR-3188 might be a potential target for the treatment of NSCLC.
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