ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012
Downregulation of the CCK-B receptor in pancreatic cancer cells blocks proliferation and promotes apoptosis.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- A randomized phase II study of gemcitabine plus Z-360, a CCK2 receptor-selective antagonist, in patients with metastatic pancreatic cancer as compared with gemcitabine plus placebo.Cancer chemotherapy and pharmacology · 2017Trial
- Identification of gastric cancer biomarkers throughBiochemistry and biophysics reports · 2024Article
- CCK Receptor Inhibition Reduces Pancreatic Tumor Fibrosis and Promotes Nanoparticle Delivery.Biomedicines · 2024Article
- Vaccination with Polyclonal Antibody Stimulator (PAS) Prevents Pancreatic Carcinogenesis in the KRAS Mouse Model.Cancer prevention research (Philadelphia, Pa.) · 2021Article
- Cholecystokinin type 2 receptor in colorectal cancer: diagnostic and therapeutic target.Journal of cancer research and clinical oncology · 2020Article
- Insights into Effects/Risks of Chronic Hypergastrinemia and Lifelong PPI Treatment in Man Based on Studies of Patients with Zollinger-Ellison Syndrome.International journal of molecular sciences · 2019Review
- Targeting cholecystokinin-2 receptor for pancreatic cancer chemoprevention.Molecular carcinogenesis · 2019Article
- Cholecystokinin receptor antagonist alters pancreatic cancer microenvironment and increases efficacy of immune checkpoint antibody therapy in mice.Cancer immunology, immunotherapy : CII · 2018Article
- Cholecystokinin Receptor-Targeted Polyplex Nanoparticle Inhibits Growth and Metastasis of Pancreatic Cancer.Cellular and molecular gastroenterology and hepatology · 2018Article
- Exploiting cancer's phenotypic guise against itself: targeting ectopically expressed peptide G-protein coupled receptors for lung cancer therapy.Oncotarget · 2017Review
- Gastrin and Gastric Cancer.Cellular and molecular gastroenterology and hepatology · 2017Review
- A Cholecystokinin B Receptor-Specific DNA Aptamer for Targeting Pancreatic Ductal Adenocarcinoma.Nucleic acid therapeutics · 2017Article
- Glucose regulates the intrinsic inflammatory response of the heart to surgically induced hypothermic ischemic arrest and reperfusion.Physiological genomics · 2017Article
- The Role of Gastrin and CCK Receptors in Pancreatic Cancer and other Malignancies.International journal of biological sciences · 2016Review
- Distribution of cholecystokinin-B receptor genotype between patients with pancreatic cancer and controls and its impact on survival.Pancreas · 2015Article
- Characterization of differentially expressed genes involved in pathways associated with gastric cancer.PloS one · 2015Article
- Novel strategies for managing pancreatic cancer.World journal of gastroenterology · 2014Review
- Cholecystokinin receptor antagonist halts progression of pancreatic cancer precursor lesions and fibrosis in mice.Pancreas · 2014Article
- Article
- Cholecystokinin and pancreatic cancer: the chicken or the egg?American journal of physiology. Gastrointestinal and liver physiology · 2014Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Gastrin stimulates the growth of pancreatic cancer cells through the activation of the cholecystokinin-B receptor (CCK-BR), which has been found to be overexpressed in pancreatic cancer. In this study, we proposed that the CCK-BR drives growth of pancreatic cancer; hence, interruption of CCK-BR activity could potentially be an ideal target for cancer therapeutics. The effect of CCK-BR downregulation in the human pancreatic adenocarcinoma cells was examined by utilizing specific CCK-BR-targeted RNA interference reagents. The CCK-BR receptor expression was both transiently and stably downregulated by transfection with selective CCK-BR small-interfering RNA or short-hairpin RNA, respectively, and the effects on cell growth and apoptosis were assessed. CCK-BR downregulation resulted in reduced cancer cell proliferation, decreased DNA synthesis, and cell cycle arrest as demonstrated by an inhibition of G(1) to S phase progression. Furthermore, CCK-BR downregulation increased caspase-3 activity, TUNEL-positive cells, and decreased X-linked inhibitor of apoptosis protein expression, suggesting apoptotic activity. Pancreatic cancer cell mobility was decreased when the CCK-BR was downregulated, as assessed by a migration assay. These results show the importance of the CCK-BR in regulation of growth and apoptosis in pancreatic cancer. Strategies to decrease the CCK-BR expression and activity may be beneficial for the development of new methods to improve the treatment for patients with pancreatic cancer.
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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.