ArticleCellular oncology (Dordrecht, Netherlands)2014
ARID3B expression in primary breast cancers and breast cancer-derived cell lines.
Article in Cellular oncology (Dordrecht, Netherlands), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- Arid3b suppresses CD8 + T cell infiltration and function in microsatellite-stable colorectal cancer via Runx3.Nature communications · 2026Article
- Serine 89 Phosphorylation Controls Nuclear Localization and Transcriptional Activity of ARID3B.Cells · 2026Article
- Article
- RGS3 acts as a tumor promoter by facilitating the regulation of the TGF-β signaling pathway and promoting EMT in ovarian cancer.Cell death discovery · 2025Article
- Article
- ARID3B: a Novel Regulator of the Kaposi's Sarcoma-Associated Herpesvirus Lytic Cycle.Journal of virology · 2016Article
- KLF15 in breast cancer: a novel tumor suppressor?Cellular oncology (Dordrecht, Netherlands) · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundARID3B (AT-rich interaction domain 3) is a member of the family of ARID proteins, which constitutes evolutionarily conserved transcription factors implicated in normal development, differentiation, cell cycle regulation and chromatin remodeling. In addition, ARID3B has been linked to cellular immortalization, epithelial-mesenchymal transition (EMT) and tumorigenesis. Given the emerging role of ARID3B in tumor development, we examined its expression in primary patient-derived breast cancer samples and breast cancer-derived cell lines.
methodsImmunohistochemistry (IHC) was used to detect ARID3B expression in 63 formalin-fixed paraffin-embedded (FFPE) invasive breast cancer samples. In addition, a panel of 6 (estrogen receptor-positive and -negative, ERBB2-positive and -negative) breast cancer-derived cell lines and immortalized non-tumorigenic epithelial breast cells were used for ARID3B expression analysis using RT-PCR. Specific primers and Western blotting were used to detect ARID3B isoforms.
resultsUsing IHC, nuclear, cytoplasmic and low levels of membranous ARID3B staining were detected in all 63 primary invasive breast tumors. Nuclear ARID3B staining positively correlated with estrogen receptor (ER) status and negatively correlated with tumor grade, mitotic index and ERBB2 status of the patients. Increased nuclear expression of ARID3B was confirmed in breast cancer-derived cell lines expressing ERα. In addition, two out of three ERBB2-positive breast cancer cell lines were found to lack full length ARID3B. Three ARID3B isoforms were found to be present in normal breast epithelial cells as well as in breast cancer cells.
conclusionWe report a positive correlation between ER positivity and nuclear ARID3B expression in primary breast cancers, along with a negative correlation with the ERBB2 status. Very similar correlations were noted in breast cancer-derived cell lines. Since in the recent past ARID3B expression has increasingly been related to cancer-associated proteins and microRNAs, knowledge on ARID3B expression and function may be instrumental for gaining further insight into potentially important cancer-related networks.
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