ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2011
Melatonin exerts by an autocrine loop antiproliferative effects in cholangiocarcinoma: its synthesis is reduced favoring cholangiocarcinoma growth.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 57 citations in OpenAlex.
- Therapeutic Potential of Melatonin in Gastrointestinal Cancers: Molecular Mechanisms, Preclinical Evidence and Clinical Implications.Journal of pineal research · 2026Review
- Melatonin-Mediated Nrf2 Activation as a Potential Therapeutic Strategy in Mutation-Driven Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Moving forward in the treatment of cholangiocarcinoma.World journal of gastrointestinal oncology · 2021Review
- Cholangiocarcinoma: bridging the translational gap from preclinical to clinical development and implications for future therapy.Expert opinion on investigational drugs · 2021Review
- Melatonin as an Antitumor Agent against Liver Cancer: An Updated Systematic Review.Antioxidants (Basel, Switzerland) · 2021Review
- Melatonin and circadian rhythms in liver diseases: Functional roles and potential therapies.Journal of pineal research · 2020Review
- Cholangiocarcinoma: novel therapeutic targets.Expert opinion on therapeutic targets · 2020Review
- Review
- Possible application of melatonin treatment in human diseases of the biliary tract.American journal of physiology. Gastrointestinal and liver physiology · 2019Review
- Immune-pineal axis - acute inflammatory responses coordinate melatonin synthesis by pinealocytes and phagocytes.British journal of pharmacology · 2018Review
- miR-24 Inhibition Increases Menin Expression and Decreases Cholangiocarcinoma Proliferation.The American journal of pathology · 2017Article
- Inhibition of the apelin/apelin receptor axis decreases cholangiocarcinoma growth.Cancer letters · 2017Article
- Structure and Functional Diversity of GCN5-Related N-Acetyltransferases (GNAT).International journal of molecular sciences · 2016Review
- miR-34a-dependent overexpression of Per1 decreases cholangiocarcinoma growth.Journal of hepatology · 2016Article
- Development and functional characterization of extrahepatic cholangiocyte lines from normal rats.Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · 2015Article
- Prolonged exposure of cholestatic rats to complete dark inhibits biliary hyperplasia and liver fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Secretin stimulates biliary cell proliferation by regulating expression of microRNA 125b and microRNA let7a in mice.Gastroenterology · 2014Article
- Overexpression of membrane metalloendopeptidase inhibits substance P stimulation of cholangiocarcinoma growth.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Melatonin regulation of biliary functions.Hepatobiliary surgery and nutrition · 2014Review
- Inhibition of the liver expression of arylalkylamine N-acetyltransferase increases the expression of angiogenic factors in cholangiocytes.Hepatobiliary surgery and nutrition · 2014Article
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
Abstract
Cholangiocarcinoma (CCA) is a devastating biliary cancer. Melatonin is synthesized in the pineal gland and peripheral organs from serotonin by two enzymes, serotonin N-acetyltransferase (AANAT) and acetylserotonin O-methyltransferase (ASMT). Cholangiocytes secrete neuroendocrine factors, including serotonin-regulating CCA growth by autocrine mechanisms. Melatonin exerts its effects by interaction with melatonin receptor type 1A/1B (MT1/MT2) receptors. We propose that 1) in CCA, there is decreased expression of AANAT and ASMT and secretion of melatonin, changes that stimulate CCA growth; and 2) in vitro overexpression of AANAT decreases CCA growth. We evaluated the 1) expression of AANAT, ASMT, melatonin, and MT1/MT2 in human nonmalignant and CCA lines and control and CCA biopsy samples; 2) melatonin levels in nonmalignant and CCA lines, and bile and serum from controls and patients with intrahepatic CCA; 3) effect of melatonin on the growth and expression of AANAT/ASMT and MT1/MT2 in CCA lines implanted into nude mice; and 4) effect of AANAT overexpression on the proliferation, apoptosis, and expression of MT1/MT2 in Mz-ChA-1 cells. The expression of AANAT, ASMT, and melatonin decreased, whereas MT1/MT2 expression increased in CCA lines and biopsy samples. Melatonin secretion decreased in the supernatant of CCA lines and bile of CCA patients. Melatonin decreased xenograft CCA tumor growth in nude mice by increased AANAT/ASMT and melatonin, along with reduced MT1/MT2 expression. Overexpression of AANAT in Mz-ChA-1 cells inhibited proliferation and MT1/MT2 expression and increased apoptosis. There is dysregulation of the AANAT/ASMT/melatonin → melatonin receptor axis in CCA, which inhibited melatonin secretion and subsequently enhanced CCA growth.
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