ArticleClinical & experimental metastasis2013
Walker 256 tumour cells increase substance P immunoreactivity locally and modify the properties of the blood-brain barrier during extravasation and brain invasion.
Article in Clinical & experimental metastasis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Crosstalk Between the Nervous System and Colorectal Cancer.Neuroscience bulletin · 2025Review
- Article
- The Effect of SP/NK1R on the Expression and Activity of Catalase and Superoxide Dismutase in Glioblastoma Cancer Cells.Biochemistry research international · 2021Article
- The Neurokinin-1 Receptor Antagonist Aprepitant: An Intelligent Bullet against Cancer?Cancers · 2020Review
- Dynamic urinary proteomic analysis in a Walker 256 intracerebral tumor model.Cancer medicine · 2019Article
- Homotypic endothelial nanotubes induced by wheat germ agglutinin and thrombin.Scientific reports · 2018Article
- Substance P Receptor Signaling Mediates Doxorubicin-Induced Cardiomyocyte Apoptosis and Triple-Negative Breast Cancer Chemoresistance.BioMed research international · 2016Article
- High expression of substance P and its receptor neurokinin-1 receptor in colorectal cancer is associated with tumor progression and prognosis.OncoTargets and therapy · 2016Article
- The substance P/NK-1 receptor system: NK-1 receptor antagonists as anti-cancer drugs.Journal of biosciences · 2015Review
- Involvement of substance P and the NK-1 receptor in pancreatic cancer.World journal of gastroenterology · 2014Review
- Article
- ASYMMETRIC CELL DIVISION: IMPLICATIONS FOR GLIOMA DEVELOPMENT AND TREATMENT.Translational neuroscience · 2013Article
- Characterisation of Walker 256 breast carcinoma cells from two tumour cell banks as assessed using two models of secondary brain tumours.Cancer cell international · 2013Article
- Why does melanoma metastasize into the brain? Genes with pleiotropic effects might be the key.Frontiers in genetics · 2013Article
- Blocking neurogenic inflammation for the treatment of acute disorders of the central nervous system.International journal of inflammation · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is not yet known how tumour cells traverse the blood-brain barrier (BBB) to form brain metastases. Substance P (SP) release is a key component of neurogenic inflammation which has been recently shown to increase the permeability of the BBB following CNS insults, making it a possible candidate as a mediator of tumour cell extravasation into the brain. This study investigated the properties of the BBB in the early stages of tumour cell invasion into the brain, and the possible involvement of SP. Male Wistar rats were injected with Walker 256 breast carcinoma cells via the internal carotid artery and euthanised at 1, 3, 6 and 9 days post tumour inoculation. Culture medium-injected animals served as controls at 1 and 9 days. Evidence of tumour cell extravasation across the BBB was first observed at 3 days post-inoculation, which corresponded with significantly increased albumin (p < 0.05) and SP immunoreactivity (p < 0.01) and significantly reduced endothelial barrier antigen labelling of microvessels when compared to culture medium control animals (p < 0.001). By day 9 after tumour cell inoculation, 100 % of animals developed large intracranial neoplasms that had significantly increased albumin in the peri-tumoral area (p < 0.001). The increased SP immunoreactivity and altered BBB properties at 3 days post-inoculation that coincided with early tumour invasion may be indicative of a mechanism for tumour cell extravasation into the brain. Thus, extravasation of tumour cells into the brain to form cerebral metastases may be a SP-mediated process.
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