ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2014
Overexpression of membrane metalloendopeptidase inhibits substance P stimulation of cholangiocarcinoma growth.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- The Repurposing of Non-Peptide Neurokinin-1 Receptor Antagonists as Antitumor Drugs: An Urgent Challenge for Aprepitant.International journal of molecular sciences · 2023Review
- Comparison of growth features and cancer stem cell prevalence in intrahepatic and extrahepatic cholangiocarcinoma cell lines.Clinical and experimental hepatology · 2022Article
- Epigenetic study of early breast cancer (EBC) based on DNA methylation and gene integration analysis.Scientific reports · 2022Article
- Recent discoveries in microbiota dysbiosis, cholangiocytic factors, and models for studying the pathogenesis of primary sclerosing cholangitis.Open medicine (Warsaw, Poland) · 2022Review
- Article
- Knockout of the Tachykinin Receptor 1 in the Mdr2The American journal of pathology · 2020Article
- The Neurokinin-1 Receptor Antagonist Aprepitant: An Intelligent Bullet against Cancer?Cancers · 2020Review
- Review
- Epidermal growth factor-like domain multiple 7 (EGFL7): Expression and possible effect on biliary epithelium growth in cholangiocarcinoma.European journal of histochemistry : EJH · 2018Article
- Inflammation and the Gut-Liver Axis in the Pathophysiology of Cholangiopathies.International journal of molecular sciences · 2018Review
- Mechanisms of cholangiocyte responses to injury.Biochimica et biophysica acta. Molecular basis of disease · 2018Review
- Recent advances in understanding bile duct remodeling and fibrosis.F1000Research · 2018Review
- Substance P increases liver fibrosis by differential changes in senescence of cholangiocytes and hepatic stellate cells.Hepatology (Baltimore, Md.) · 2017Article
- Potential Expanded Indications for Neprilysin Inhibitors.Current heart failure reports · 2017Review
- Long-term neprilysin inhibition - implications for ARNIs.Nature reviews. Cardiology · 2017Review
- BCAT1 expression associates with ovarian cancer progression: possible implications in altered disease metabolism.Oncotarget · 2015Article
- The substance P/NK-1 receptor system: NK-1 receptor antagonists as anti-cancer drugs.Journal of biosciences · 2015Review
- Neurokinin-1 receptor antagonists as antitumor drugs in gastrointestinal cancer: A new approach.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology AssociationReview
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
Substance P (SP) promotes cholangiocyte growth during cholestasis by activating its receptor, NK1R. SP is a proteolytic product of tachykinin (Tac1) and is deactivated by membrane metalloendopeptidase (MME). This study aimed to evaluate the functional role of SP in the regulation of cholangiocarcinoma (CCA) growth. NK1R, Tac1, and MME expression and SP secretion were assessed in human CCA cells and nonmalignant cholangiocytes. The proliferative effects of SP (in the absence/presence of the NK1R inhibitor, L-733,060) and of L-733,060 were evaluated. In vivo, the effect of L-733,060 treatment or MME overexpression on tumor growth was evaluated by using a xenograft model of CCA in nu/nu nude mice. The expression of Tac1, MME, NK1R, PCNA, CK-19, and VEGF-A was analyzed in the resulting tumors. Human CCA cell lines had increased expression of Tac1 and NK1R, along with reduced levels of MME compared with nonmalignant cholangiocytes, resulting in a subsequent increase in SP secretion. SP treatment increased CCA cell proliferation in vitro, which was blocked by L-733,060. Treatment with L-733,060 alone inhibited CCA proliferation in vitro and in vivo. Xenograft tumors derived from MME-overexpressed human Mz-ChA-1 CCA cells had a slower growth rate than those derived from control cells. Expression of PCNA, CK-19, and VEGF-A decreased, whereas MME expression increased in the xenograft tumors treated with L-733,060 or MME-overexpressed xenograft tumors compared with controls. The study suggests that SP secreted by CCA promotes CCA growth via autocrine pathway. Blockade of SP secretion and NK1R signaling may be important for the management of CCA.
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Registered trials
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.