ArticleCell death & disease2021
TFAP2A potentiates lung adenocarcinoma metastasis by a novel miR-16 family/TFAP2A/PSG9/TGF-β signaling pathway.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 68 citations in OpenAlex.
- TFAP2A enhances radioresistance of non-small cell lung cancer by transcriptionally activating BRCA1 : TFAP2A promotes NSCLC radioresistance.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Crosstalk between lactylation and other post-translational modifications in health and diseases.Molecular biomedicine · 2026Review
- TFAP2A-Induced Upregulation of LncRNA NUTM2A-AS1 Promotes LUAD Progression Through a miR-409-5p/SLC35F2 Regulatory Axis.Journal of cellular and molecular medicine · 2026Article
- Article
- TFAP2A regulates SGPP2 transcription to promote lipid accumulation and activate the Wnt/β-catenin signaling pathway to promote malignant progression in lung adenocarcinoma.Journal of translational medicine · 2026Article
- CES3 promotes NSCLC progression via lipid metabolic reprogramming regulated by TFAP2A.Journal of Cancer · 2026Article
- Interaction of TFAP2A with the Ku70/80 complex is crucial for HIF-dependent activation of hypoxia-inducible genes.The FEBS journal · 2025Article
- TFAP2A facilitates the metastasis and radioresistance of esophageal cancer by promoting EGFR transcription.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- TFAP2A upregulates FAM83A to suppress ferroptosis and diminish cisplatin sensitivity in non-small cell lung cancer.Cell division · 2025Article
- IGF2BP3 suppresses ferroptosis in lung adenocarcinoma by m6A-dependent regulation of TFAP2A to transcriptionally activate SLC7A11/GPX4.Molecular and cellular biochemistry · 2025Article
- HNRNPC promotes progression of non-small cell lung cancer by maintaining TFAP2A mRNA stability.Cancer cell international · 2025Article
- CENPF (+) cancer cells promote malignant progression of early-stage TP53 mutant lung adenocarcinoma.Oncogenesis · 2025Article
- Integration of single-cell and bulk RNA sequencing to identify a distinct tumor stem cells and construct a novel prognostic signature for evaluating prognosis and immunotherapy in LUAD.Journal of translational medicine · 2025Article
- TFAP2A drives non-small cell lung cancer (NSCLC) progression and resistance to targeted therapy by facilitating the ESR2-mediated MAPK pathway.Cell death discovery · 2024Article
- The molecular features of lung cancer stem cells in dedifferentiation process-driven epigenetic alterations.The Journal of biological chemistry · 2024Review
- Single-cell transcriptome analysis reveals evolving tumour microenvironment induced by immunochemotherapy in nasopharyngeal carcinoma.Clinical and translational medicine · 2024Article
- Article
- The effect of TFAP2A/ANXA8 axis on ferroptosis of cervical squamous cell carcinoma (CESC) in vitro.Cytotechnology · 2024Article
- TFAP2A downregulation mediates tumor-suppressive effect of miR-8072 in triple-negative breast cancer via inhibiting SNAI1 transcription.Breast cancer research : BCR · 2024Article
- CRTAC1 identified as a promising diagnosis and prognostic biomarker in lung adenocarcinoma.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription factor AP-2α (TFAP2A) was previously regarded as a critical regulator during embryonic development, and its mediation in carcinogenesis has received intensive attention recently. However, its role in lung adenocarcinoma (LUAD) has not been fully elucidated. Here, we tried to investigate TFAP2A expression profiling, clinical significance, biological function and molecular underpinnings in LUAD. We proved LUAD possessed universal TFAP2A high expression, indicating a pervasively poorer prognosis in multiple independent datasets. Then we found TFAP2A was not indispensable for LUAD proliferation, and exogenous overexpression even caused repression. However, we found TFAP2A could potently promote LUAD metastasis possibly by triggering epithelial-mesenchymal transition (EMT) in vitro and in vivo. Furthermore, we demonstrated TFAP2A could transactivate Pregnancy-specific glycoprotein 9 (PSG9) to enhance transforming growth factor β (TGF-β)-triggering EMT in LUAD. Meanwhile, we discovered suppressed post-transcriptional silencing of miR-16 family upon TFAP2A partly contributed to TFAP2A upregulation in LUAD. In clinical specimens, we also validated cancer-regulating effect of miR-16 family/TFAP2A/PSG9 axis, especially for lymph node metastasis of LUAD. In conclusion, we demonstrated that TFAP2A could pivotally facilitate LUAD progression, possibly through a novel pro-metastasis signaling pathway (miR-16 family/TFAP2A/PSG9/ TGF-β).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.