ArticleLaboratory investigation; a journal of technical methods and pathology2012
Monoamine oxidase A expression is suppressed in human cholangiocarcinoma via coordinated epigenetic and IL-6-driven events.
Article in Laboratory investigation; a journal of technical methods and pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 68 citations in OpenAlex.
- Chronic alcohol consumption sex-dependently affects IL-6 modulation of GABAergic synapses in the central amygdala of rhesus macaques.Brain, behavior, and immunity · 2026Article
- Transcriptional Activity of Genes Related to the Biotransformation Process in the Development of Colorectal Cancer.International journal of molecular sciences · 2025Article
- MAOB promotes ROS-mediated DNA damage, triggering a cyclic MAOB-HNF1A-53BP1-p53 axis that suppresses the malignancy of clear cell renal cell carcinoma.Redox biology · 2025Article
- The highs and lows of monoamine oxidase as molecular target in cancer: an updated review.Molecular and cellular biochemistry · 2025Review
- Targeting monoamine oxidases in cancer: advances and opportunities.Trends in molecular medicine · 2025Review
- Demystifying metabolic‒immune crosstalk: how amino acid metabolic reprogramming shapes the malignant phenotype and macrophage polarization of biliary and pancreatic tumors.International journal of biological sciences · 2025Review
- Beyond CTLA-4 and PD-1: Novel Insights into MAO-A as a Next Generation Immune Checkpoint Modulator for Cancer Immunotherapy.Current cancer drug targets · 2025Review
- MAOB expression correlates with a favourable prognosis in prostate cancer, and its genetic variants are associated with the metastasis of the disease.Journal of cellular and molecular medicine · 2024Article
- Periampullary cancer and neurological interactions: current understanding and future research directions.Frontiers in oncology · 2024Review
- Evaluation of the serotonin pathway as a biomarker in cholangiocarcinoma.Journal of gastrointestinal oncology · 2023Article
- DAGLβ is the principal synthesizing enzyme of 2-AG and promotes aggressive phenotype of intrahepatic cholangiocarcinoma via AP-1/DAGLβ/miR4516 feedforward circuitry.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- Inhibition of dopamine receptor D1 signaling promotes human bile duct cancer progression via WNT signaling.Cancer science · 2023Article
- Aberrant tryptophan metabolism in stromal cells is associated with mesenteric fibrosis in small intestinal neuroendocrine tumors.Endocrine connections · 2022Article
- Review
- Article
- α-Synuclein Up-regulates Monoamine Oxidase A Expression and ActivityFrontiers in aging neuroscience · 2021Article
- Monoamine Oxidase A Inhibits Lung Adenocarcinoma Cell Proliferation by Abrogating Aerobic Glycolysis.Frontiers in oncology · 2021Article
- The clinical value and potential molecular mechanism of the downregulation of MAOA in hepatocellular carcinoma tissues.Cancer medicine · 2020Article
- Potential monoamine oxidase A inhibitor suppressing paclitaxel-resistant non-small cell lung cancer metastasis and growth.Thoracic cancer · 2020Article
- Identification of a nine-gene prognostic signature for gastric carcinoma using integrated bioinformatics analyses.World journal of gastrointestinal oncology · 2020Article
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
The secretion of dopamine and serotonin is increased in cholangiocarcinoma, which has growth-promoting effects. Monoamine oxidase A (MAOA), the degradation enzyme of serotonin and dopamine, is suppressed in cholangiocarcinoma via an unknown mechanism. The aims of this study were to (i) correlate MAOA immunoreactivity with pathophysiological parameters of cholangiocarcinoma, (ii) determine the mechanism by which MAOA expression is suppressed and (iii) evaluate the consequences of restored MAOA expression in cholangiocarcinoma. MAOA expression was assessed in cholangiocarcinoma and nonmalignant controls. The control of MAOA expression by promoter hypermethylation was evaluated and the contribution of interleukin-6 (IL-6) signaling to the suppression of MAOA expression was determined. The effects of MAOA overexpression on cholangiocarcinoma growth and invasion were also assessed. MAOA expression is correlated with differentiation, invasion and survival in cholangiocarcinoma. The MAOA promoter was hypermethylated immediately upstream of the start codon in cholangiocarcinoma samples and cell lines but not in nonmalignant counterparts. IL-6 signaling also decreased MAOA expression via a mechanism independent of hypermethylation, involving the regulation of the balance between SP-1 transcriptional activity and its inhibitor, R1 repressor. Inhibition of both IL-6 signaling and DNA methylation restored MAOA levels to those observed in cholangiocytes. Forced MAOA overexpression inhibited cholangiocarcinoma growth and invasion. MAOA expression is suppressed by the coordinated control of promoter hypermethylation and IL-6 signaling. MAOA may be a useful prognostic marker in the management of cholangiocarcinoma, and therapies designed to increase MAOA expression might prove beneficial in the treatment of cholangiocarcinoma.
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