ArticlePloS one2011
DeltaNp63alpha-mediated induction of epidermal growth factor receptor promotes pancreatic cancer cell growth and chemoresistance.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Polymorphisms within autophagy-related genes as susceptibility biomarkers for pancreatic cancer: A meta-analysis of three large European cohorts and functional characterization.International journal of cancer · 2025Pooled it
- Basal Marker ΔNp63α Is Enriched in Pancreatic Cancer Metastases but Not in Primary Tumors Post-Chemotherapy.Cancer medicine · 2026Article
- Sensitising PDAC to Gemcitabine by Suppressing NF-κB Pathway and Enhancing Apoptosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Interaction between MED12 and ΔNp63 activates basal identity in pancreatic ductal adenocarcinoma.Nature genetics · 2024Article
- Marker-based CRISPR screening reveals a MED12-p63 interaction that activates basal identity in pancreatic ductal adenocarcinoma.bioRxiv : the preprint server for biology · 2023Article
- ΔNp63 Regulates Radioresistance in Human Head and Neck Squamous Carcinoma Cells.Current issues in molecular biology · 2023Article
- A Systemic and Integrated Analysis of p63-Driven Regulatory Networks in Mouse Oral Squamous Cell Carcinoma.Cancers · 2023Article
- The dual role of p63 in cancer.Frontiers in oncology · 2023Review
- The p53 Family Members p63 and p73 Roles in the Metastatic Dissemination: Interactions with microRNAs and TGFβ Pathway.Cancers · 2022Review
- Compressive stress-mediated p38 activation required for ERα + phenotype in breast cancer.Nature communications · 2021Article
- ERK3 is transcriptionally upregulated by ∆Np63α and mediates the role of ∆Np63α in suppressing cell migration in non-melanoma skin cancers.BMC cancer · 2021Article
- Squamous trans-differentiation of pancreatic cancer cells promotes stromal inflammation.eLife · 2020Article
- Transcriptional suppression of AMPKα1 promotes breast cancer metastasis upon oncogene activation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- FIH-1 engages novel binding partners to positively influence epithelial proliferation via p63.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- ΔNp63α promotes the expression and nuclear translocation of PTEN, leading to cisplatin resistance in oral cancer cells.American journal of translational research · 2020Article
- Clinical update on head and neck cancer: molecular biology and ongoing challenges.Cell death & disease · 2019Review
- Metformin and 4SC-202 synergistically promote intrinsic cell apoptosis by accelerating ΔNp63 ubiquitination and degradation in oral squamous cell carcinoma.Cancer medicine · 2019Article
- ΔNp63 in squamous cell carcinoma: defining the oncogenic routes affecting epigenetic landscape and tumour microenvironment.Molecular oncology · 2019Review
- Synergistic antitumour activity of HDAC inhibitor SAHA and EGFR inhibitor gefitinib in head and neck cancer: a key role for ΔNp63α.British journal of cancer · 2019Article
- IL-1β Inflammatory Cytokine-InducedInternational journal of molecular sciences · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is highly resistant to current chemotherapy regimens, in part due to alterations in the p53 tumor suppressor pathway. p53 homolog p63 is a transcription factor essential for the development and differentiation of epithelial surfaces. However its function in cancer is controversial and its role in PDAC is not known. We discovered that ΔNp63α was the predominantly expressed p63 variant in pancreatic cancer cell lines. ΔNp63α protein and mRNA levels were high in T3M4, BxPC3 and COLO-357 pancreatic cancer cells and low in ASPC-1 and PANC-1 cells. Overexpression of ΔNp63α in PANC-1 cells and shRNA-mediated knockdown in T3M4 cells indicated that ΔNp63α promoted anchorage-dependent and -independent growth, motility and invasion, and enhanced resistance to cisplatin-induced apoptosis. Epidermal growth factor receptor (EGFR) signaling pathways contribute to the biological aggressiveness of PDAC, and we found that the motogenic effects of ΔNp63α were augmented in presence of EGF. Ectopic expression of ΔNp63α resulted in upregulation of EGFR and β1-integrin in PANC-1 cells. Conversely, ΔNp63α knockdown had an opposite effect in T3M4 cells. ΔNp63α potentiated EGF-mediated activation of ERK, Akt and JNK signaling. Chromatin immunoprecipitation and functional reporter assays demonstrated that ΔNp63α activated EGFR transcription. 14-3-3σ transcription was also positively regulated by ΔNp63α and we have previously shown that 14-3-3σ contributes to chemoresistance in pancreatic cancer cell lines. Conversely, shRNA-mediated knockdown of 14-3-3σ led to abrogation of the ΔNp63α effects on cell proliferation and invasion. Thus, p53 homolog ΔNp63α enhances the oncogenic potential of pancreatic cancer cells through trans-activation of EGFR and 14-3-3σ.
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Registered trials
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.