ArticleMolecular therapy : the journal of the American Society of Gene Therapy2018
miR-296-3p Negatively Regulated by Nicotine Stimulates Cytoplasmic Translocation of c-Myc via MK2 to Suppress Chemotherapy Resistance.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 50 citations in OpenAlex.
- Different MicroRNAs expression inRNA biology · 2026Review
- Extracellular vesicles enriched with mitochondrial components from intermittently cold-exposed adipose tissue drive metabolically active adipose regeneration via miR-296-3p.Materials today. Bio · 2026Article
- C-MYC as a key effector of WNT, PI3K/AKT, MAPK, and TGF-β signaling pathways in regulation of epithelial-mesenchymal transition during tumor metastasis.Cancer cell international · 2026Review
- MK2-mediated AKT/MYC signaling activation promotes epithelial-mesenchymal transition in lung adenocarcinoma.Frontiers in genetics · 2025Article
- Long non-coding RNA MAGEA4-AS1 binding to p53 enhances MK2 signaling pathway and promotes the proliferation and metastasis of oral squamous cell carcinoma.Functional & integrative genomics · 2024Article
- Cell signaling and epigenetic regulation of nicotine-induced carcinogenesis.Environmental pollution (Barking, Essex : 1987) · 2024Review
- Non-coding RNA and drug resistance in head and neck cancer.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- The promising role of miRNAs in radioresistance and chemoresistance of nasopharyngeal carcinoma.Frontiers in oncology · 2024Review
- Nicotine Suppresses Phagocytic Ability of Macrophages by Regulating the miR-296-3p-SIRPAnalytical cellular pathology (Amsterdam) · 2023Article
- MiRNA signatures in nasopharyngeal carcinoma: molecular mechanisms and therapeutic perspectives.American journal of cancer research · 2023Review
- Nicotine-induced miR-21-3p promotes chemoresistance in lung cancer by negatively regulating FOXO3a.Oncology letters · 2022Article
- miR-3682-3p directly targets FOXO3 and stimulates tumor stemness in hepatocellular carcinomaWorld journal of stem cells · 2022Article
- Mapping Research on miRNAs in Cancer: A Global Data Analysis and Bibliometric Profiling Analysis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2022Article
- lncRNA FEZF1-AS1 regulates biological behaviors of cervical cancer by targeting miRNA-1254.Food science & nutrition · 2021Article
- Review
- Current Status and Future Perspectives about Molecular Biomarkers of Nasopharyngeal Carcinoma.Cancers · 2021Review
- VPS33B interacts with NESG1 to suppress cell growth and cisplatin chemoresistance in ovarian cancer.Cancer science · 2021Article
- VPS33B suppresses lung adenocarcinoma metastasis and chemoresistance to cisplatin.Genes & diseases · 2021Article
- miR-1254 induced by NESG1 inactivates HDGF/DDX5-stimulated nuclear translocation of β-catenin and suppresses NPC metastasis.Molecular therapy. Methods & clinical development · 2021Article
- VPS33B modulates c-Myc/p53/miR-192-3p to target CCNB1 suppressing the growth of non-small cell lung cancer.Molecular therapy. Nucleic acids · 2021Article
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to identify mechanisms by which microRNA 296-3p (miR-296-3p) functions as a tumor suppressor to restrain nasopharyngeal carcinoma (NPC) cell growth, metastasis, and chemoresistance. Mechanistic studies revealed that miR-296-3p negatively regulated by nicotine directly targets the oncogenic protein mitogen-activated protein kinase-activated protein kinase-2 (Mapkapk2) (MK2). Suppression of MK2 downregulated Ras/Braf/Erk/Mek/c-Myc and phosphoinositide-3-kinase (PI3K)/Akt/c-Myc signaling and promoted cytoplasmic translocation of c-Myc, which activated miR-296-3p expression by a feedback loop. This ultimately inhibited cell cycle progression, epithelial-to-mesenchymal transition (EMT), and chemoresistance of NPC. In addition, nicotine as a key component of tobacco was observed to suppress miR-296-3p and thus elevate MK2 expression by inducing PI3K/Akt/c-Myc signaling. In clinical samples, reduced miR-296-3p as an unfavorable factor was inversely correlated with MK2 and c-Myc expression. These results reveal a novel mechanism by which miR-296-3p negatively regulated by nicotine directly targets MK2-induced Ras/Braf/Erk/Mek/c-Myc or PI3K/AKT/c-Myc signaling to stimulate its own expression and suppress NPC cell proliferation and metastasis. miR-296-3p may thus serve as a therapeutic target to reverse chemotherapy resistance of NPC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.