ArticleCell death & disease2020
TFAP2C facilitates somatic cell reprogramming by inhibiting c-Myc-dependent apoptosis and promoting mesenchymal-to-epithelial transition.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- The RNA-binding protein La/SSB is associated with HNSCC progression and TFAP2C/FSCN1-linked transcriptional regulation.Oncogene · 2026Article
- All-Flex Plasma Patch for In Vivo Delivery of Reactive Species.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Propofol attenuates angiogenesis by activating endoplasmic reticulum stress to suppress TFAP2C-driven VEGFA transcription.Apoptosis : an international journal on programmed cell death · 2026Article
- Single-cell multi-omics analysis reveals cancer regulatory elements of transcriptional programs and clinical implications.Cell death & disease · 2025Article
- A genome-wide analysis of YY1 and TFAP2 competition on overlapping motifs reveals their roles in HPV-induced carcinogenesis.PLoS pathogens · 2025Article
- Deciphering the role of cis-regulatory elements and TFAP2C in the activation of zygotic Sox2 expression in mouse preimplantation embryos.Development (Cambridge, England) · 2025Article
- TFAP2C activates PTGES through the NOTCH3 signaling pathway to affect gefitinib resistance in lung adenocarcinoma.Journal of clinical biochemistry and nutrition · 2025Article
- The mitochondrial unfolded protein response inhibits pluripotency acquisition and mesenchymal-to-epithelial transition in somatic cell reprogramming.Nature metabolism · 2025Article
- TFAP2C-DDR1 axis regulates resistance to CDK4/6 inhibitor in breast cancer.Cancer letters · 2025Article
- HDAC4/MybL1/YAP novel signaling axis is required for pancreatic cancer metastasis to the liver.International journal of biological sciences · 2025Article
- Prediction of NR3C1 as a methylation marker for the prevention and treatment of gastric cancer in Rhizoma Atractylodis Macrocephalae based on machine learning algorithm and bioinformatics analysis.Frontiers in genetics · 2025Article
- Reconstitution of pluripotency from mouse fibroblast through Sall4 overexpression.Nature communications · 2024Article
- Chromatin landscape dynamics during reprogramming towards human naïve and primed pluripotency reveals the divergent function of PRDM1 isoforms.Cell death discovery · 2024Article
- Human iPSC-derived neural stem cells displaying radial glia signature exhibit long-term safety in mice.Nature communications · 2024Article
- An endothelial regulatory module links blood pressure regulation with elite athletic performance.PLoS genetics · 2024Article
- Regulation of Enhancers by SUMOylation Through TFAP2C Binding and Recruitment of HDAC Complex to the Chromatin.Research square · 2024Article
- The transcriptional regulatory network modulating human trophoblast stem cells to extravillous trophoblast differentiation.Nature communications · 2024Article
- The occurrence and development of induced pluripotent stem cells.Frontiers in genetics · 2024Review
- WD repeat domain 48 promotes hepatocellular carcinoma progression by stabilizing c-Myc.Journal of cellular and molecular medicine · 2022Article
- TFAP2C Knockdown Sensitizes Bladder Cancer Cells to Cisplatin Treatment via Regulation of EGFR and NF-κB.Cancers · 2022Article
Corrections and comments
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription factors are known to mediate the conversion of somatic cells to induced pluripotent stem cells (iPSCs). Transcription factor TFAP2C plays important roles in the regulation of embryonic development and carcinogenesis; however, the roles of Tfap2c in regulating somatic cell reprogramming are not well understood. Here we demonstrate Tfap2c is induced during the generation of iPSCs from mouse fibroblasts and acts as a facilitator for iPSCs formation. Mechanistically, the c-Myc-dependent apoptosis, which is a roadblock to reprogramming, can be significantly mitigated by Tfap2c overexpression. Meanwhile, Tfap2c can greatly promote mesenchymal-to-epithelial transition (MET) at initiation stage of OSKM-induced reprogramming. Further analysis of gene expression and targets of Tfap2c during reprogramming by RNA-sequencing (RNA-seq) and ChIP-qPCR indicates that TFAP2C can promote epithelial gene expression by binding to their promoters directly. Finally, knockdown of E-cadherin (Cdh1), an important downstream target of TFAP2C and a critical regulator of MET antagonizes Tfap2c-mediated reprogramming. Taken together, we conclude that Tfap2c serves as a strong activator for somatic cell reprogramming through promoting the MET and inhibiting c-Myc-dependent apoptosis.
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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.