ArticleOncology research2017
Silencing of Armadillo Repeat-Containing Protein 8 (ARMc8) Inhibits TGF-β-Induced EMT in Bladder Carcinoma UMUC3 Cells.
Article in Oncology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Comprehensive analysis of the expression and prognostic value of ARMCs in pancreatic adenocarcinoma.BMC cancer · 2025Article
- MiR-455-3p inhibits gastric cancer progression by repressing Wnt/β-catenin signaling through binding to ARMC8.BMC medical genomics · 2023Article
- Effects of the uremic toxin indoxyl sulphate on human microvascular endothelial cells.Journal of applied toxicology : JAT · 2022Article
- Article
- ARMC Subfamily: Structures, Functions, Evolutions, Interactions, and Diseases.Frontiers in molecular biosciences · 2021Review
- Transcription factor YY1 mediates epithelial-mesenchymal transition through the TGFβ signaling pathway in bladder cancer.Medical oncology (Northwood, London, England) · 2020Article
- Review
- Armc8 is an evolutionarily conserved armadillo protein involved in cell-cell adhesion complexes through multiple molecular interactions.Bioscience reports · 2019Article
- The micro RNA hsa-miR-377-3p inhibits tumor growth in malignant melanoma.RSC advances · 2019Article
- Clinicohistopathological implications of phosphoserine 9 glycogen synthase kinase-3β/ β-catenin in urinary bladder cancer patients.World journal of clinical oncology · 2019Article
- The CTLH Complex in Cancer Cell Plasticity.Journal of oncology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Armadillo repeat-containing protein 8 (ARMc8) is a key factor in regulating cell migration, proliferation, tissue maintenance, and tumorigenesis. However, its role in bladder cancer remains unknown. Thus, in this study we sought to investigate the effect of ARMc8 on the epithelial-to-mesenchymal transition (EMT) progress in bladder cancer cells induced by transforming growth factor-β1 (TGF-β1). Our results found that ARMc8 was highly expressed in bladder cancer cell lines. ARMc8 silencing inhibited the TGF-β1-induced migration and invasion and suppressed the EMT progress in bladder cancer cells. Furthermore, ARMc8 silencing inhibited the TGF-β1-induced expression of β-catenin, cyclin D1, and c-myc in bladder cancer cells. In conclusion, the present study demonstrates a novel function for ARMc8, which acts as a mediator for TGF-β1-induced cell migration/invasion through modulation of the Wnt/β-catenin signaling pathway in bladder cancer cells. This study suggests that ARMc8 may be a potential therapeutic target for the development of therapies for bladder 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.