ArticleCell death discovery2024
TFAP2A drives non-small cell lung cancer (NSCLC) progression and resistance to targeted therapy by facilitating the ESR2-mediated MAPK pathway.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed.
- Multi-omic cell free DNA profiles of cerebral spinal fluid from lung cancer metastasis to the brain.NAR cancer · 2026Article
- miR-135a-5p exerts tumor-suppressive effects in 769P renal carcinoma cells through the TFAP2A/KRT8 signaling axis.In vitro cellular & developmental biology. Animal · 2026Article
- Acquired resistance of cancer therapies: Mechanisms and perspectives.Chinese medical journal · 2026Review
- TFAP2A transcriptionally regulates B3GALT2 to affect gouty arthritis progression through pyroptosis: a study based on machine learning and multi-omics integration analysis.Journal of orthopaedic surgery and research · 2026Article
- Article
- Nanopore-based cell-free DNA fragmentation and methylation profiles from the cerebral spinal fluid of patients with lung cancer brain metastases.bioRxiv : the preprint server for biology · 2025Article
- TFAP2A upregulates FAM83A to suppress ferroptosis and diminish cisplatin sensitivity in non-small cell lung cancer.Cell division · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Cancer is among the leading causes of death related diseases worldwide, and lung cancer has the highest mortality rate in the world. Transcription factors (TFs) constitute a class of structurally and functionally intricate proteins. Aberrant expression or functional deficiencies of transcription factors may give rise to abnormal gene expression, contributing to various diseases, including tumours. In this study, we propose to elucidate the potential role and mechanism of TFAP2A in NSCLC. We found that TFAP2A levels were significantly greater in tumour tissues than para-tumour tissues, and high expression of TFAP2A was associated with poor prognosis in NSCLC patients. Additionally, TFAP2A overexpression promoted NSCLC progression both in vivo and in vitro. Mechanistically, ESR2 is a potential target regulated by TFAP2A and that TFAP2A can bind to the promoter region of ESR2. Furthermore, the overexpression of both TFAP2A and ESR2 in NSCLC cells was associated with the overactivation of MAPK signalling, and the combination of PHTPP and osimertinib had a synergistic effect on suppressing tumour growth.
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Registered trials
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