ArticleMolecular medicine reports2017
MicroRNA-146a promotes gastric cancer cell apoptosis by targeting transforming growth factor β-activated kinase 1.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Non-coding RNAs as potential therapeutic targets for receptor tyrosine kinase signaling in solid tumors: current status and future directions.Cancer cell international · 2024Review
- Fluid shear stress-induced down-regulation of miR-146a-5p inhibits osteoblast apoptosis via targeting SMAD4.Physiological research · 2022Article
- GRAMD4 inhibits tumour metastasis by recruiting the E3 ligase ITCH to target TAK1 for degradation in hepatocellular carcinoma.Clinical and translational medicine · 2021Article
- Anti-Hepatocellular Carcinoma Biomolecules: Molecular Targets Insights.International journal of molecular sciences · 2021Review
- Cascades between miRNAs, lncRNAs and the NF-κB signaling pathway in gastric cancer (Review).Experimental and therapeutic medicine · 2021Review
- MicroRNA in Gastric Cancer Development: Mechanisms and Biomarkers.Diagnostics (Basel, Switzerland) · 2020Review
- Review
- TAK1 regulates endothelial cell necroptosis and tumor metastasis.Cell death and differentiation · 2019Article
- Expression profile of microRNA-146a along HPV-induced multistep carcinogenesis: a study in HPV16 transgenic mice.Journal of cancer research and clinical oncology · 2018Article
- MicroRNA Roles in the Nuclear Factor Kappa B Signaling Pathway in Cancer.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence suggests that microRNA (miR)-146a functions as an oncogene or tumor suppressor in various cancers. However, the role of miR‑146a in gastric cancer (GC) remains to be elucidated. The present study investigated the function of miR‑146a in GC cells. The results of the present study revealed that miR‑146a modulates GC cell apoptosis. Overexpression of miR‑146a significantly increased apoptosis of SGC‑7901 cells, whereas inhibition of miR‑146a protected cells from apoptosis. miR‑146a expression in GC cells was inversely correlated with transforming growth factor β‑activated kinase 1 (TAK1) expression, at the mRNA and protein levels. Furthermore, small interfering RNA‑mediated silencing of TAK1 enhanced GC cell apoptosis, whereas overexpression of TAK1 promoted survival of GC cells. Overexpression of miR‑146a or knockdown of TAK1 led to a marked increase in inhibitor of κBα (IκBα) and a decrease in B‑cell lymphoma 2 (Bcl‑2) expression levels in SGC‑7901 cells. By contrast, silencing of miR‑146a or TAK1 overexpression downregulated IκBα and upregulated Bcl‑2 expression levels. Therefore, the results of the present study demonstrated a novel negative feedback mechanism to promote GC cell apoptosis involving the miR‑146a/TAK1/nuclear factor-κB axis.
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