ArticleOncotarget2014
COX-2 overexpression increases malignant potential of human glioma cells through Id1.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Clinicopathological and prognostic significance of cyclooxygenase-2 expression in head and neck cancer: A meta-analysis.Oncotarget · 2016Pooled it
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- Micheliolide suppresses the viability, migration and invasion of U251MG cells via the NF-κB signaling pathway.Oncology letters · 2020Article
- Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines.Cancer cell international · 2020Article
- Cyclooxygenase (COX) Inhibition by Acetyl Salicylic Acid (ASA) Enhances Antitumor Effects of Nitric Oxide in Glioblastoma In Vitro.Molecular neurobiology · 2019Article
- Small-molecule inhibition of prostaglandin E receptor 2 impairs cyclooxygenase-associated malignant glioma growth.British journal of pharmacology · 2019Article
- Discovery and Therapeutic Exploitation of Mechanisms of Resistance to MET Inhibitors in Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Drug Repurposing of Metabolic Agents in Malignant Glioma.International journal of molecular sciences · 2018Review
- A drug combination targeting hypoxia induced chemoresistance and stemness in glioma cells.Oncotarget · 2018Article
- Inhibitor of DNA binding proteins: implications in human cancer progression and metastasis.American journal of translational research · 2018Review
- Aberrantly activated Cox-2 and Wnt signaling interact to maintain cancer stem cells in glioblastoma.Oncotarget · 2017Article
- Cyclooxygenase-2 Induction by Amino Acid Deprivation Requires p38 Mitogen-Activated Protein Kinase in Human Glioma Cells.Cancer investigation · 2017Article
- Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma.Journal of neuro-oncology · 2017Article
- Parecoxib inhibits glioblastoma cell proliferation, migration and invasion by upregulating miRNA-29c.Biology open · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased COX-2 expression directly correlates with glioma grade and is associated with shorter survival in glioblastoma (GBM) patients. COX-2 is also regulated by epidermal growth factor receptor signaling which is important in the pathogenesis of GBMs. However, COX-2 expression has not been previously shown to directly alter malignancy of GBMs. Id1 is a member of the helix-loop-helix (HLH) family of transcriptional repressors that act as dominant-negative inhibitors of basic-HLH factors. This factor has been shown to be regulated by COX-2 in breast carcinoma cells and recent studies suggest that Id1 may also be involved in the genesis/progression of gliomas. We now show that COX-2 increases the aggressiveness of GBM cells. GBM cells with COX-2 overexpression show increased growth of colonies in soft agar. Tumorigenesis in vivo is also increased in both subcutaneous flank and orthotopic intracranial tumor models. COX-2 overexpression induces Id1 expression in two GBM cell lines suggesting a role for Id1 in glioma transformation/tumorigenesis. Furthermore, we find direct evidence of a role for Id1 with significant suppression of in vitro transformation and in vivo tumorigenesis in COX-2-overexpressing GBM cells where Id1 has been knocked down. In fact, Id1 is even more efficient at enhancing transformation/tumorigenesis of GBM cells than COX-2. Finally, GBM cells with COX-2 or Id1 overexpression show greater migration/invasive potential and tumors that arise from these cells also display increased microvessel density, results in line with the increased malignant potential seen in these cells. Thus, COX-2 enhances the malignancy of GBM cells through induction of Id1.
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