ReviewSeminars in cancer biology2008
Bench to bedside and back again: molecular mechanisms of alpha-catenin function and roles in tumorigenesis.
Review in Seminars in cancer biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
74 citing papers in PubMed, 129 citations in OpenAlex.
- Variant-specific functional effects of CTNNA1 in a humanized Drosophila model.European journal of human genetics : EJHG · 2026Article
- Article
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- Multiscale mechanical-adapted hydrogels for the repair of intervertebral disc degeneration.Bioactive materials · 2025Article
- Current advances and challenges in Managing Hereditary Diffuse Gastric Cancer (HDGC): a narrative review.Hereditary cancer in clinical practice · 2024Review
- TheProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Anoikis resistance--protagonists of breast cancer cells survive and metastasize after ECM detachment.Cell communication and signaling : CCS · 2023Review
- α-catenin interaction with YAP/FoxM1/TEAD-induced CEP55 supports liver cancer cell migration.Cell communication and signaling : CCS · 2023Article
- Distinct inter-domain interactions of dimeric versus monomeric α-catenin link cell junctions to filaments.Communications biology · 2023Article
- Insights into the Structure and Function of TRIP-1, a Newly Identified Member in Calcified Tissues.Biomolecules · 2023Article
- Hereditary Diffuse Gastric Cancer: A 2022 Update.Journal of personalized medicine · 2022Review
- mEpigenetics · 2022Article
- Roads to Stat3 Paved with Cadherins.Cells · 2022Review
- Adherens junction proteins on the move-From the membrane to the nucleus in intestinal diseases.Frontiers in cell and developmental biology · 2022Review
- Tumor-suppressor function of Beclin 1 in breast cancer cells requires E-cadherin.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Role of α-Catenin and its mechanosensing properties in regulating Hippo/YAP-dependent tissue growth.PLoS genetics · 2019Article
- Targeting Cell Adhesion Molecules via Carbonate Apatite-Mediated Delivery of Specific siRNAs to Breast Cancer Cells In Vitro and In Vivo.Pharmaceutics · 2019Article
- Untangling the response of bone tumor cells and bone forming cells to matrix stiffness and adhesion ligand density by means of hydrogels.Biomaterials · 2019Article
- αE-catenin is a candidate tumor suppressor for the development of E-cadherin-expressing lobular-type breast cancer.The Journal of pathology · 2018Article
- Analysis of a vinculin homolog in a sponge (phylum Porifera) reveals that vertebrate-like cell adhesions emerged early in animal evolution.The Journal of biological chemistry · 2018Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The cadherin/catenin complex, comprised of E-cadherin, beta-catenin and alpha-catenin, is essential for initiating cell-cell adhesion, establishing cellular polarity and maintaining tissue organization. Disruption or loss of the cadherin/catenin complex is common in cancer. As the primary cell-cell adhesion protein in epithelial cells, E-cadherin has long been studied in cancer progression. Similarly, additional roles for beta-catenin in the Wnt signaling pathway has led to many studies of the role of beta-catenin in cancer. Alpha-catenin, in contrast, has received less attention. However, recent data demonstrate novel functions for alpha-catenin in regulating the actin cytoskeleton and cell-cell adhesion, which when perturbed could contribute to cancer progression. In this review, we use cancer data to evaluate molecular models of alpha-catenin function, from the canonical role of alpha-catenin in cell-cell adhesion to non-canonical roles identified following conditional alpha-catenin deletion. This analysis identifies alpha-catenin as a prognostic factor in cancer progression.
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What 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.