ArticlePloS one2013
Loss of CLCA4 promotes epithelial-to-mesenchymal transition in breast cancer cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
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Who cites it
47 citing papers in PubMed, 58 citations in OpenAlex.
- Dedifferentiation-driven oncogenic stemness promotes tumor-sustaining adaptability in the intestinal epithelium.Cell death & disease · 2026Article
- The impact of disease and species differences on the intestinal CLCA4 gene expression.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Predicting gene signature in breast cancer patients with multiple machine learning models.Discover oncology · 2024Article
- Weighted gene co-expression network analysis for hub genes in colorectal cancer.Pharmacological reports : PR · 2024Article
- Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on ClInternational journal of molecular sciences · 2023Review
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- PI3K/AKT signaling pathway as a critical regulator of epithelial-mesenchymal transition in colorectal tumor cells.Cell communication and signaling : CCS · 2023Review
- CLCA2 overexpression suppresses epithelial-to-mesenchymal transition in cervical cancer cells through inactivation of ERK/JNK/p38-MAPK signaling pathways.BMC molecular and cell biology · 2022Article
- Epithelial-mesenchymal transition process during embryo implantation.Cell and tissue research · 2022Review
- <em>miR-19a</em> targeting <em>CLCA4</em> to regulate the proliferation, migration, and invasion of colorectal cancer cells.European journal of histochemistry : EJH · 2022Article
- Proteomic analysis distinguishes extracellular vesicles produced by cancerous versus healthy pancreatic organoids.Scientific reports · 2022Article
- Chloride Channels and Transporters: Roles beyond Classical Cellular Homeostatic pH or Ion Balance in Cancers.Cancers · 2022Review
- Identification of Hub Genes in Colorectal Adenocarcinoma by Integrated Bioinformatics.Frontiers in cell and developmental biology · 2022Article
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- The epithelial sodium channel has a role in breast cancer cell proliferation.Breast cancer research and treatment · 2021Article
- Microenvironment Stiffness Amplifies Post-ischemia Heart Regeneration in Response to Exogenous Extracellular Matrix Proteins in Neonatal Mice.Frontiers in cardiovascular medicine · 2021Article
- Expression of the CLCA4 Gene in Esophageal Carcinoma and Its Impact on the Biologic Function of Esophageal Carcinoma Cells.Journal of oncology · 2021Article
- The Diagnostic and Prognostic Roles of Combined Expression of Novel Biomarkers in Lung Adenocarcinoma and Lung Squamous Cell Carcinoma: An Immunohistochemical Study.Iranian journal of pathology · 2021Article
- Mutation profiling in eight cases of vagal paragangliomas.BMC medical genomics · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The epithelial to mesenchymal transition (EMT) is a developmental program in which epithelial cells downregulate their cell-cell junctions, acquire spindle cell morphology and exhibit cellular motility. In breast cancer, EMT facilitates invasion of surrounding tissues and correlates closely with cancer metastasis and relapse. We found previously that the candidate tumor suppressor CLCA2 is expressed in differentiated, growth-arrested mammary epithelial cells but is downregulated during tumor progression and EMT. We further demonstrated that CLCA2 is a p53-inducible proliferation-inhibitor whose loss indicates an increased risk of metastasis. We show here that another member of the CLCA gene family, CLCA4, is expressed in mammary epithelial cells and is similarly downregulated in breast tumors and in breast cancer cell lines. Like CLCA2, the gene is stress-inducible, and ectopic expression inhibits colony formation. Transcriptional profiling studies revealed that CLCA4 and CLCA2 together are markers for mammary epithelial differentiation, and both are downregulated by TGF beta. Moreover, knockdown of CLCA4 in immortalized cells by shRNAs caused downregulation of epithelial marker E-cadherin and CLCA2, while mesenchymal markers N-cadherin, vimentin, and fibronectin were upregulated. Double knockdown of CLCA2 and CLCA4 enhanced the mesenchymal profile. These findings suggest that CLCA4 and CLCA2 play complementary but distinct roles in epithelial differentiation. Clinically, low expression of CLCA4 signaled lower relapse-free survival in basal and luminal B breast cancers.
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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.