ArticleThe Journal of biological chemistry2013
Neurokinin-1 receptor directly mediates glioma cell migration by up-regulation of matrix metalloproteinase-2 (MMP-2) and membrane type 1-matrix metalloproteinase (MT1-MMP).
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 46 citations in OpenAlex.
- The GPCR Connection: Linking Alzheimer's Disease and Glioblastoma.Journal of cellular and molecular medicine · 2026Review
- Anti-Metastatic Effects of Aprepitant on Glioblastoma Cells: Targeting the Substance P/Neurokinin-1 Pathway.Cancer medicine · 2025Article
- Review
- Aprepitant inhibits the development and metastasis of gallbladder cancer via ROS and MAPK activation.BMC cancer · 2023Article
- The effect of substance P and its specific antagonist (aprepitant) on the expression of MMP-2, MMP-9, VEGF, and VEGFR in ovarian cancer cells.Molecular biology reports · 2022Article
- Neurotransmitters: Potential Targets in Glioblastoma.Cancers · 2022Review
- Discovery of a New CaMKII-Targeted Synthetic Lethal Therapy against Glioblastoma Stem-like Cells.Cancers · 2022Article
- Neurokinin-1 receptor promotes non-small cell lung cancer progression through transactivation of EGFR.Cell death & disease · 2022Article
- The Neurokinin-1 Receptor Is Essential for the Viability of Human Glioma Cells: A Possible Target for Treating Glioblastoma.BioMed research international · 2022Article
- Lactate induced up-regulation of KLHDC8A (Kelch domain-containing 8A) contributes to the proliferation, migration and apoptosis of human glioma cells.Journal of cellular and molecular medicine · 2020Article
- The Neurokinin-1 Receptor Antagonist Aprepitant: An Intelligent Bullet against Cancer?Cancers · 2020Review
- The NK-1R Antagonist Aprepitant Prevents LPS-Induced Oxidative Stress and Inflammation in RAW264.7 Macrophages.Drug design, development and therapy · 2020Article
- LncRNA RMRP silence curbs neonatal neuroblastoma progression by regulating microRNA-206/tachykinin-1 receptor axis via inactivating extracellular signal-regulated kinases.Cancer biology & therapy · 2019Article
- LncRNA ZNF503-AS1 promotes RPE differentiation by downregulating ZNF503 expression.Cell death & disease · 2017Article
- β-Arrestin 1 has an essential role in neurokinin-1 receptor-mediated glioblastoma cell proliferation and GThe Journal of biological chemistry · 2017Article
- RNA-Sequencing Analysis of Messenger RNA/MicroRNA in a Rabbit Aneurysm Model Identifies Pathways and Genes of Interest.AJNR. American journal of neuroradiology · 2015Article
- G protein-coupled receptors as oncogenic signals in glioma: emerging therapeutic avenues.Neuroscience · 2014Review
- The tetraspanin CD81 protein increases melanoma cell motility by up-regulating metalloproteinase MT1-MMP expression through the pro-oncogenic Akt-dependent Sp1 activation signaling pathways.The Journal of biological chemistry · 2014Article
- Proton beam irradiation stimulates migration and invasion of human U87 malignant glioma cells.Journal of radiation research · 2014Article
- Tachykinins and their receptors: contributions to physiological control and the mechanisms of disease.Physiological reviews · 2014Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurokinin-1 receptor (NK1R) occurs naturally on human glioblastomas. Its activation mediates glioma cell proliferation. However, it is unknown whether NK1R is directly involved in tumor cell migration. In this study, we found human hemokinin-1 (hHK-1), via NK1R, dose-dependently promoted the migration of U-251 and U-87 cells. In addition, we showed that hHK-1 enhanced the activity of MMP-2 and the expression of MMP-2 and MT1-matrix metalloproteinase (MMP), which were responsible for cell migration, because neutralizing the MMPs with antibodies decreased cell migration. The involved mechanisms were then investigated. In U-251, hHK-1 induced significant calcium efflux; phospholipase C inhibitor U-73122 reduced the calcium mobilization, the up-regulation of MMP-2 and MT1-MMP, and the cell migration induced by hHK-1, which meant the migration effect of NK1R was mainly mediated through the G(q)-PLC pathway. We further demonstrated that hHK-1 boosted rapid phosphorylation of ERK, JNK, and Akt; inhibition of ERK and Akt effectively reduced MMP-2 induction by hHK-1. Meanwhile, inhibition of ERK, JNK, and Akt reduced the MT1-MMP induction. hHK-1 stimulated significant phosphorylation of p65 and c-JUN in U-251. Reporter gene assays indicated hHK-1 enhanced both AP-1 and NF-κB activity; inhibition of ERK, JNK, and Akt dose-dependently suppressed the NF-κB activity; only the inhibition of ERK significantly suppressed the AP-1 activity. Treatment with specific inhibitors for AP-1 or NF-κB strongly blocked the MMP up-regulation by hHK-1. Taken together, our data suggested NK1R was a potential regulator of human glioma cell migration by the up-regulation of MMP-2 and MT1-MMP.
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