ArticleBreast cancer research : BCR2024
TFAP2A downregulation mediates tumor-suppressive effect of miR-8072 in triple-negative breast cancer via inhibiting SNAI1 transcription.
Article in Breast cancer research : BCR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Mapping the Subtype-Specific PARP1 ADP-Ribosylated Proteome in Breast Cancer Cells.Molecular cancer research : MCR · 2026Article
- Lnc RNA GAPLINC affects triple-negative breast cancer progression through the miR-331-3p/IGF2BP1 axis.World journal of surgical oncology · 2026Article
- TFAP2A-mediated Transcriptional Activation of ELMO1 Inhibits Ferroptosis and Promotes Esophageal Squamous Cell Carcinoma Progression.Molecular biotechnology · 2026Article
- Anoikis classification of lung squamous cell carcinoma reveals correlation with clinical prognosis and immune characteristics.Annals of medicine · 2025Article
- Formononetin, a Key Component of Danggui Buxue Decoction, Inhibits Metastasis of Triple-Negative Breast Cancer by Modulating SNAI2-Driven EMT.Food science & nutrition · 2025Article
- Epigenetic profiling reveals key super-enhancer networks driving oncogenesis in HPV-positive HNSCC.iScience · 2025Article
- TFAP2A induces cisplatin resistance via BNIP3-mediated mitophagy in non-small cell lung cancer.Translational cancer research · 2025Article
- Mapping the Subtype-Specific PARP1 ADP-ribosylated Proteome in Breast Cancer Cells.bioRxiv : the preprint server for biology · 2025Article
- TFAP2A facilitates the metastasis and radioresistance of esophageal cancer by promoting EGFR transcription.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Curcumenol inhibits malignant progression and promotes ferroptosis via the SLC7A11/NF‑κB/TGF‑β pathway in triple‑negative breast cancer.International journal of molecular medicine · 2025Article
- Molecular targets and therapies associated with poor prognosis of triple‑negative breast cancer (Review).International journal of oncology · 2025Review
- IGF2BP3 suppresses ferroptosis in lung adenocarcinoma by m6A-dependent regulation of TFAP2A to transcriptionally activate SLC7A11/GPX4.Molecular and cellular biochemistry · 2025Article
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Abstract
backgroundTriple-negative breast cancer (TNBC) represents a highly aggressive subset of breast malignancies characterized by its challenging clinical management and unfavorable prognosis. While TFAP2A, a member of the AP-2 transcription factor family, has been implicated in maintaining the basal phenotype of breast cancer, its precise regulatory role in TNBC remains undefined.
methodsIn vitro assessments of TNBC cell growth and migratory potential were conducted using MTS, colony formation, and EdU assays. Quantitative PCR was employed to analyze mRNA expression levels, while Western blot was utilized to evaluate protein expression and phosphorylation status of AKT and ERK. The post-transcriptional regulation of TFAP2A by miR-8072 and the transcriptional activation of SNAI1 by TFAP2A were investigated through luciferase reporter assays. A xenograft mouse model was employed to assess the in vivo growth capacity of TNBC cells.
resultsSelective silencing of TFAP2A significantly impeded the proliferation and migration of TNBC cells, with elevated TFAP2A expression observed in breast cancer tissues. Notably, TNBC patients exhibiting heightened TFAP2A levels experienced abbreviated overall survival. Mechanistically, TFAP2A was identified as a transcriptional activator of SNAI1, a crucial regulator of epithelial-mesenchymal transition (EMT) and cellular proliferation, thereby augmenting the oncogenic properties of TFAP2A in TNBC. Moreover, miR-8072 was unveiled as a negative regulator of TFAP2A, exerting potent inhibitory effects on TNBC cell growth and migration. Importantly, the tumor-suppressive actions mediated by the miR-8072/TFAP2A axis were intricately associated with the attenuation of AKT/ERK signaling cascades and the blockade of EMT processes.
conclusionsOur findings unravel the role and underlying molecular mechanism of TFAP2A in driving tumorigenesis of TNBC. Targeting the TFAP2A/SNAI1 pathway and utilizing miR-8072 as a suppressor represent promising therapeutic strategies for treating TNBC.
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