ArticleFrontiers in pharmacology2018
Inhibiting β-Catenin by β-Carboline-Type MDM2 Inhibitor for Pancreatic Cancer Therapy.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
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- Biophysical Survey of Small-Molecule β-Catenin Inhibitors: A Cautionary Tale.Journal of medicinal chemistry · 2022Review
- Cross-Talk between p53 and Wnt Signaling in Cancer.Biomolecules · 2022Review
- Design, synthesis, and biological characterization of a potent STAT3 degrader for the treatment of gastric cancer.Frontiers in pharmacology · 2022Article
- Inhibition of STAT3 Signaling Pathway by Terphenyllin Suppresses Growth and Metastasis of Gastric Cancer.Frontiers in pharmacology · 2022Article
- Convergent Canonical Pathways in Autism Spectrum Disorder from Proteomic, Transcriptomic and DNA Methylation Data.International journal of molecular sciences · 2021Review
- The roles and regulation of MDM2 and MDMX: it is not just about p53.Genes & development · 2021Review
- Targeting the p53-MDM2 pathway for neuroblastoma therapy: Rays of hope.Cancer letters · 2021Review
- Targeting MDM2 for Neuroblastoma Therapy: In Vitro and In Vivo Anticancer Activity and Mechanism of Action.Cancers · 2020Article
- Review
- Terphenyllin Suppresses Orthotopic Pancreatic Tumor Growth and Prevents Metastasis in Mice.Frontiers in pharmacology · 2020Article
- Antimicrobial Peptide Reverses ABCB1-Mediated Chemotherapeutic Drug Resistance.Frontiers in pharmacology · 2020Article
- Targeting β-Catenin Signaling by Natural Products for Cancer Prevention and Therapy.Frontiers in pharmacology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The β-catenin and MDM2 oncoproteins are overexpressed and constitutively activated in human pancreatic cancer and contribute to its initiation, progression, and metastasis. The Wnt/β-catenin signaling pathway strongly interacts with the MDM2-p53 signaling pathway, accelerating the tumorigenesis and its development. Therefore, therapies inhibiting both β-catenin and MDM2 are suggested to be ideal treatments for patients with advanced pancreatic cancer. We have recently identified a novel class of β-carboline compounds as the specific and potent MDM2 inhibitors, including a lead compound SP141. In the present study, we utilized SP141 as an exemplary β-carboline compound to characterize β-catenin as a molecular target of the β-carboline compounds and to demonstrate an important role of β-catenin in the anticancer activity of β-carboline. We found that the silencing of either β-catenin or MDM2 largely reduced the anticancer activity of SP141 while the double silencing of both genes almost completely blocked SP141's activity. SP141 directly bound to β-catenin and inhibited its expression and activity in pancreatic cancer cells
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