ArticleOncology letters2014
Anticancer activities of sulindac in prostate cancer cells associated with c-Jun NH2-terminal kinase 1/β-catenin signaling.
Article in Oncology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Modulation of JNK-1/ β-catenin signaling byRSC advances · 2019Article
- A small diversity library of α-methyl amide analogs of sulindac for probing anticancer structure-activity relationships.Bioorganic & medicinal chemistry letters · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The non-steroidal anti-inflammatory agent, sulindac, has shown strong effects on cancer prevention in colorectal cancers, however, its anticancer activities on prostate cancer remain unclear. In the current study, human prostate cancer cell lines, LNCaP and PC-3, were treated with various concentrations of sulindac and it was found that sulindac significantly inhibits prostate cancer cell proliferation and promotes cell apoptosis in a dose- and time-dependent manner. Further studies revealed that sulindac significantly induces c-Jun NH2-terminal kinase (JNK) 1 phosphorylation and inhibits β-catenin at the transcriptional and post-transcriptional levels. In conclusion, by targeting the JNK1/β-catenin signaling pathway, sulindac may present a potential preventive or therapeutic agent for treatment of patients with prostate 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.