ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014
A novel NF-κB/MMP-3 signal pathway involves in the aggressivity of glioma promoted by Bmi-1.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Genetic Variants of BMI1 (rs1042059 and rs11591377) and Their Potential Role in Leukemia Susceptibility: A Narrative Review.Health science reports · 2026Article
- MMP3 at the crossroads: Linking molecular pathways to disease diagnosis and therapy.Pharmacological research · 2025Review
- Insights Into the Role of Bmi-1 Deregulation in Promoting Stemness and Therapy Resistance in Glioblastoma: A Narrative Review.Cancer medicine · 2025Review
- The Role of the NF-kB Pathway in Intracranial Aneurysms.Brain sciences · 2023Review
- Prognostic utility of TME-associated genes in pancreatic cancer.Frontiers in genetics · 2023Article
- The Crucial Roles of Bmi-1 in Cancer: Implications in Pathogenesis, Metastasis, Drug Resistance, and Targeted Therapies.International journal of molecular sciences · 2022Review
- Article
- Corilagin Induces High Levels of Apoptosis in the Temozolomide-Resistant T98G Glioma Cell Line.Oncology research · 2018Article
- The mechanism study of lentiviral vector carrying methioninase enhances the sensitivity of drug-resistant gastric cancer cells to Cisplatin.British journal of cancer · 2018Article
- Bmi‑1‑targeting suppresses osteosarcoma aggressiveness through the NF‑κB signaling pathway.Molecular medicine reports · 2017Article
- Pyrrolidine dithiocarbamate sensitizes U251 brain glioma cells to temozolomide via downregulation ofOncology letters · 2017Article
- Bmi-1 serves as a potential novel marker for progression in human cutaneous basal cell carcinoma.International journal of clinical and experimental pathology · 2017Article
- Nuclear matrix metalloproteinases: functions resemble the evolution from the intracellular to the extracellular compartment.Cell death discovery · 2017Review
- The Interplay of Reactive Oxygen Species, Hypoxia, Inflammation, and Sirtuins in Cancer Initiation and Progression.Oxidative medicine and cellular longevity · 2016Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Matrix metalloproteinase 3 (MMP-3) is implicated in the pathogenesis and progression of glioma. However, whether MMP-3 participates in the regulation of metastasis and its mechanisms in glioma is mostly unknown. In the present study, glioma cells were stably transfected with Bmi-1 small interfering RNA (siRNA) to knockdown off Bmi-1 or were transiently transfected with Bmi-1 complementary DNA (cDNA) to upregulate the Bmi-1 level and to evaluate their effects on invasion and expression analysis for molecules involved in invasion. Knockdown of Bmi-1 dramatically reduced a nuclear factor kappa B (NF-κB) and MMP-3 expression and activity in T98G cells. When the T98G cells were upregulated in the Bmi-1 levels, the T98G cells were treated with 10 μM BAY 11-7028 to inhibit the NF-κB activity. The invasion induced by upregulation of Bmi-1 was severely abolished by BAY 11-7028 in Bmi-1 overexpression cells. The T98G cell metastatic potential was increased by overexpression of Bmi-1; completely at the same time, the NF-κB activity and MMP-3 expression was also increased. Taken together, these findings suggest that Bmi-1 promotes glioma cell migration and invasion via NF-κB-mediated upregulation of MMP-3.
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