ArticleMolecular biotechnology2023
SAFB2 Inhibits the Progression of Breast Cancer by Suppressing the Wnt/β-Catenin Signaling Pathway via NFAT5.
Article in Molecular biotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06438055 (Clinical Treatment of Refractory Breast Cancer Based on Organoid Drug Sensitivity Results), which is not on this map. Cited by 3 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.
Clinical Treatment of Refractory Breast Cancer Based on Organoid Drug Sensitivity Results
Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- [Expression of NFAT5 and IGF1R in nasopharyngeal carcinoma tissues and analysis of clinical characteristics].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2025Article
- SUMOylation substrate encoding genes as prognostic biomarkers in pancreatic ductal adenocarcinoma with functional assessment ofFrontiers in pharmacology · 2025Article
- Rel Family Transcription Factor NFAT5 Upregulates COX2 via HIF-1α Activity in Ishikawa and HEC1a Cells.International journal of molecular sciences · 2024Article
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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
Aberrant scaffold attachment factor-B2 (SAFB2) expression is associated with several malignant tumors. In this study, we investigated how SAFB2 worked in the process of breast cancer as well as the underlying mechanism. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting analysis were used to investigate the expression of SAFB2 and nuclear factor of activated T cells 5 (NFAT5). Cellular proliferative ability was detected with cell counting kit 8 (CCK8), colony formation and 5-Ethynyl-2'-deoxyuridine (EdU) staining assays. Cell apoptosis was measured via flow cytometry and western blotting analysis. Wound healing, transwell assays, and western blotting analysis were executed to estimate cell migration and invasion. The relationship between SAFB2 and NFAT5 was verified by RNA immunoprecipitation (RIP) assay and NFAT5 mRNA stability was examined with actinomycin (Act) D assay. Western blotting analysis also tested the expression of Wnt/β-catenin signaling-associated proteins. As a result, SAFB2 was downregulated in breast cancer cell lines, while NFAT5 was highly expressed in most breast cancer cell lines. Overexpression of SAFB2 suppressed the proliferation, migration, and invasion while exacerbated the apoptosis of breast cancer cells. SAFB2 interacted with NFAT5 mRNA and declined the stability of NFAT5 mRNA. Overexpression of NFAT5 counteracted anti-proliferative, anti-metastatic and pro-apoptotic effects of SAFB2 in breast cancer cells. Mechanistically, SAFB2 overexpression inhibited the Wnt/β-catenin signaling pathway, while this effect was partially eliminated by NFAT5. Collectively, SAFB2 hindered breast cancer development and inactivated Wnt/β-catenin signaling via regulation of NFAT5, suggesting that SAFB2 might be a promising therapeutic target for breast cancer.
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