ArticleJournal of molecular signaling2012
Chibby suppresses growth of human SW480 colon adenocarcinoma cells through inhibition of β-catenin signaling.
Article in Journal of molecular signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Attenuation of Wnt signaling by miR-27a-5p-GFPT2-HBP axis via metabolic reprogramming in colorectal cancer.Biology direct · 2026Article
- Combined Chibby and β-Catenin Predicts Clinical Outcomes in Patients with Hepatocellular Carcinoma.International journal of molecular sciences · 2020Article
- Anti-oncogenic activity of Chibby in the development of human nasopharyngeal carcinoma.Oncology letters · 2018Article
- Downregulation of nuclear and cytoplasmic Chibby is associated with advanced cervical cancer.Oncology letters · 2017Article
- Chibby1 knockdown promotes mesenchymal-to-epithelial transition-like changes.Cell cycle (Georgetown, Tex.) · 2017Article
- The high expression of TC1 (C8orf4) was correlated with the expression of β-catenin and cyclin D1 and the progression of squamous cell carcinomas of the tongue.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Article
- 14-3-3 and β-catenin are secreted on extracellular vesicles to activate the oncogenic Wnt pathway.Molecular oncology · 2014Article
- BCR-ABL1-associated reduction of beta catenin antagonist Chibby1 in chronic myeloid leukemia.PloS one · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The canonical Wnt signaling pathway is crucial for embryonic development and adult tissue homeostasis. Activating mutations in the Wnt pathway are frequently associated with the pathogenesis of various types of cancer, particularly colon cancer. Upon Wnt stimulation, β-catenin plays a central role as a coactivator through direct interaction with Tcf/Lef transcription factors to stimulate target gene expression. We have previously shown that the evolutionarily conserved protein Chibby (Cby) physically binds to β-catenin to repress β-catenin-dependent gene activation by 1) competing with Tcf/Lef factors for binding to β-catenin and 2) facilitating nuclear export of β-catenin via interaction with 14-3-3 proteins. In this study, we employed human colon adenocarcinoma SW480 cells with high levels of endogenous β-catenin to address a potential tumor suppressor role of Cby. In SW480 stable cells expressing wild-type Cby (CbyWT), but not 14-3-3-binding- defective Cby mutant CbyS20A, a significant fraction of endogenous β-catenin was detected in the cytoplasm. Consistent with this, CbyWT-expressing cells showed low levels of β-catenin signaling activity, leading to reduced growth. Our results suggest that Cby, in collaboration with 14-3-3 proteins, can counteract oncogenic β-catenin signaling in colon cancer cells.
Identifiers
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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.