ArticleiScience2025
TAF7 directly targets SAA1 to enhance triple-negative breast cancer metastasis via phosphorylating E-cadherin and N-cadherin.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Myeloid-derived suppressor cells in cancer: biology, regulatory networks and theranostic prospects.Signal transduction and targeted therapy · 2026Review
- Single-cell RNA sequencing reveals that TAF7 promotes colorectal cancer stemness by targeting SOX2.Biology direct · 2026Article
- TAF7 accumulates in the cytoplasm during cellular transformation and engages STAT3, WASH, and CCT.Frontiers in cell and developmental biology · 2026Article
- Single-cell transcriptomics in metastatic breast cancer: mapping tumor evolution and therapeutic resistance.Frontiers in genetics · 2025Review
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Authors and funding
15 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Identification of metastasis drivers of triple-negative breast cancer (TNBC) is a multifaceted challenge. Here, we identified TATA-box binding protein associated factor 7 (TAF7) as a candidate to modulate TNBC metastasis. TAF7 exhibited high expression in metastatic TNBC patients, and its elevated expression showed a negative correlation with overall survival in TNBC patients. The knockdown of TAF7 suppressed the migration and invasion of TNBC, suggesting TAF7 plays a role in the metastatic processes. Further, TAF7 was enhancing serum amyloid A1 (SAA1) transcription by binding to a specific motif in the SAA1 gene promoter. The elevated SAA1 in TNBC cells directly increased E-cadherin and N-cadherin phosphorylation thereby regulating cell adhesion. Mechanistically, TAF7 modulated cell invasion, migration, and lung metastasis through an SAA1-dependent manner
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