ArticlePharmaceutics2021
A Novel N-Sulfonylamidine-Based Derivative Inhibits Proliferation, Migration, and Invasion in Human Colorectal Cancer Cells by Suppressing Wnt/β-Catenin Signaling Pathway.
Article in Pharmaceutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wnt signaling has been implicated in the development and metastasis of colorectal cancer (CRC), as well as poorer outcomes. Thus, targeting the Wnt/β-catenin signaling pathway is expected to be a promising treatment option for the therapy of advanced metastatic CRC. A new N-sulfonylamidine derivative (26ag) has been confirmed to suppress the growth of tumor cells by inhibiting C-met, showing strong anti-cancer activity. In this paper, we test the effectiveness of 26ag in suppressing CRC cell proliferation, invasion, and migration. In this regard, 26ag decreased the mRNA and protein expressions of important hallmarks associated with epithelial to mesenchymal transition (EMT). Furthermore, we provide evidence that β-catenin-dependent signaling is involved in 26ag-induced Wnt/β-catenin pathway effects in CRC, using in vitro cell culture and computer docking models. Our study indicates that inhibition of Wnt/β-catenin by a novel compound, 26ag, demonstrates possibility for drug development in the therapy of CRC.
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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.