ArticleAmerican journal of translational research2017
The crosstalk between β-catenin signaling and type I, type II and type III interferons in lung cancer cells.
Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
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- The role of Wnt/β-catenin signaling in lung cancer progression and therapy: a comprehensive review.Medical oncology (Northwood, London, England) · 2025Review
- B7-H3 in Pediatric Tumors: Far beyond Neuroblastoma.Cancers · 2023Review
- Associations Between Single Nucleotide Polymorphisms of Hypoxia-Related Genes and Capsule Formation in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2023Article
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- Transcriptional Analyses Identify Genes That Modulate Bovine Macrophage Response toFrontiers in cellular and infection microbiology · 2020Article
- A meta-analysis and bioinformatics exploration of the diagnostic value and molecular mechanism of miR-193a-5p in lung cancer.Oncology letters · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectiveIFNs induce potent antiviral and antitumor activities. β-catenin pathway is a surviving pathway adapted by carcinogenetic mechanisms of various cancers. Crosstalk between these pathways has not been well described in lung cancer cells.
methodsLung cancer cell lines, A549 and Calu-3, were used in this study. β-catenin protein levels and signaling activities were tested by flow cytometry and luciferase assay. Cell proliferation was measured by counting viable cells under microscope, and apoptosis by TUNEL assay and caspase 3 activation. DKK1 and GSK3β levels were tested by flow cytometry. Secreted DKK1 was measured by ELISA. αDKK1 , FLUD and S3I were to inhibit DKK1, STAT1 and STAT3 activities, respectively.
resultsAll of IFNα, IFNγ and IFNλ1 suppressed β-catenin signaling in A549 and Calu-3 cells, where IFNγ was the strongest (P<0.05). They inhibited cellular proliferation and promoted apoptosis. IFNγ gave greater induction ability compared to IFNα and IFNλ1 (P<0.05). All tested IFNs promoted DKK1 activation but not GSK3β in A549 and Calu-3 cells. IFNs activated STAT1 and STAT3. But only STAT3 was vital for IFN-mediated DKK1 activation and apoptosis. Plus, DKK1 antagonist abrogated IFN-mediated apoptosis. The degree of STAT3 activation was corresponding to the level of apoptosis induced by different IFNs (P<0.05).
conclusionsIn lung cancer cells, all three types of IFNs can induce apoptosis via suppressing β-catenin signaling by a STAT3- and DKK1-dependent manner. This findings demonstrate a link between IFNs and β-catenin signaling, which may possess potentials on the development of novel therapeutic measures against lung cancer.
Indexed as
Identifiers
28670369PMC5489881W2923249203What OpenQuestion holds
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.