ArticleTechnology in cancer research & treatment2017
MiR-98 Promotes Apoptosis of Glioma Cells via Suppressing IKBKE/NF-κB Pathway.
Article in Technology in cancer research & treatment, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Identifying Key Pathogenic Mechanisms in Recurrent Glioblastoma Through Bioinformatics Analysis.Current medicinal chemistry · 2026Article
- Article
- IKBKE modulates autophagy and progestin resistance in endometrial cancer.Frontiers in oncology · 2025Article
- MAPK signaling pathway-based glioma subtypes, machine-learning risk model, and key hub proteins identification.Scientific reports · 2023Article
- LIN28B and Let-7 in Diffuse Midline Glioma: A Review.Cancers · 2023Review
- Inhibition of NF-κB activation by BAY 11-7821 suppresses the proliferation and inflammation of glioma cells through inducing autophagy.Translational cancer research · 2022Article
- miRNA-451 regulates the NF-κB signaling pathway by targeting IKKβ to inhibit glioma cell growth.Cell cycle (Georgetown, Tex.) · 2021Article
- MicroRNA-4500 Inhibits Migration, Invasion, and Angiogenesis of Breast Cancer Cells via RRM2-Dependent MAPK Signaling Pathway.Molecular therapy. Nucleic acids · 2020Article
- Article
- microRNA-98 protects sepsis mice from cardiac dysfunction, liver and lung injury by negatively regulating HMGA2 through inhibiting NF-κB signaling pathway.Cell cycle (Georgetown, Tex.) · 2019Article
- MCCK1 enhances the anticancer effect of temozolomide in attenuating the invasion, migration and epithelial-mesenchymal transition of glioblastoma cells in vitro and in vivo.Cancer medicine · 2019Article
- MicroRNA-98 targets HMGA2 to inhibit the development of retinoblastoma through mediating Wnt/β-catenin pathway.Cancer biomarkers : section A of Disease markers · 2019Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inhibitor of kappa B kinase epsilon is overexpressed in glioma and plays antiapoptotic role via activating nuclear factor-kappa B. microRNA-98 can suppress glioma, modulate the activities of nuclear factor-kappa B, and bind to the 3'-untranslated region of inhibitor of kappa B kinase epsilon messenger RNA. This study was aimed to investigate the modulation of inhibitor of kappa B kinase epsilon/nuclear factor-kappa B by microRNA-98 in glioma. The results indicated that microRNA-98 was downregulated in glioma cell lines and human glioma tissues. Overexpression of microRNA-98 in U87MG and T98G glioma cells significantly increased the apoptosis induced by ultraviolet irradiation and suppressed nuclear factor-kappa B luciferase activity, nuclear factor-kappa B p50 subunit expression, and B-cell lymphoma-2 (Bcl-2) expression in glioma cells. Silencing inhibitor of kappa B kinase epsilon decreased the expression of nuclear factor-kappa B p50 subunit and the luciferase activity of nuclear factor-kappa B, while the nuclear factor-kappa B activity could be significantly retrieved when inhibitor of kappa B kinase epsilon was expressed in microRNA-98-transfected cells. These findings indicated that microRNA-98 could promote apoptosis of glioma cells via inhibiting inhibitor of kappa B kinase epsilon/nuclear factor-kappa B signaling and presented a novel regulatory pathway of microRNA-98 by direct suppression of inhibitor of kappa B kinase epsilon/nuclear factor-kappa B expression in glioma cells.
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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.