ArticlePancreas2015
The basic helix-loop-helix transcription factor E47 reprograms human pancreatic cancer cells to a quiescent acinar state with reduced tumorigenic potential.
Article in Pancreas, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- Transcriptomic regulation of pancreatic acinar cell homeostasis and plasticity.Biochemical Society transactions · 2026Review
- Pancreatic Acinar Cell Carcinoma: Demographics, Treatment, and Survival Outcomes, A Retrospective Population-Based Study.Journal of gastrointestinal cancer · 2025Article
- SenNet recommendations for detecting senescent cells in different tissues.Nature reviews. Molecular cell biology · 2024Review
- Deciphering cellular plasticity in pancreatic cancer for effective treatments.Cancer metastasis reviews · 2024Review
- Metastasis Models: Thermodynamics and Complexity.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Review
- Senescence program and its reprogramming in pancreatic premalignancy.Cell death & disease · 2023Review
- Review
- Pharmacological inhibition and reversal of pancreatic acinar ductal metaplasia.Cell death discovery · 2022Article
- Expression Profiles of ID and E2A in Ovarian Cancer and Suppression of Ovarian Cancer by the E2A Isoform E47.Cancers · 2022Article
- Complex Elucidation of Cells-of-Origin in Pediatric Soft Tissue Sarcoma: From Concepts to Real Life, Hide-and-Seek through Epigenetic and Transcriptional Reprogramming.International journal of molecular sciences · 2022Review
- ELAPOR1 is a secretory granule maturation-promoting factor that is lost during paligenosis.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- E47 upregulates ΔNp63α to promote growth of squamous cell carcinoma.Cell death & disease · 2021Article
- Loss of RE-1 silencing transcription factor accelerates exocrine damage from pancreatic injury.Cell death & disease · 2020Article
- Salivary glands require Aurora Kinase B for regeneration after transient innate immune-mediated injury.Scientific reports · 2019Article
- Generate TALE/TALEN as Easily and Rapidly as Generating CRISPR.Molecular therapy. Methods & clinical development · 2019Article
- Signaling Networks That Control Cellular Plasticity in Pancreatic Tumorigenesis, Progression, and Metastasis.Gastroenterology · 2019Review
- Gene activation by a CRISPR-assistedeLife · 2019Article
- MIST1, an Inductive Signal for Salivary Amylase in Mesenchymal Stem Cells.International journal of molecular sciences · 2019Article
- Inflammation and de-differentiation in pancreatic carcinogenesis.World journal of clinical cases · 2018Review
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
objectivesPancreatic ductal adenocarcinoma (PDA) initiates from quiescent acinar cells that attain a Kras mutation, lose signaling from basic helix-loop-helix (bHLH) transcription factors, undergo acinar-ductal metaplasia, and rapidly acquire increased growth potential. We queried whether PDA cells can be reprogrammed to revert to their original quiescent acinar cell state by shifting key transcription programs.
methodsHuman PDA cell lines were engineered to express an inducible form of the bHLH protein E47. Gene expression, growth, and functional studies were investigated using microarray, quantitative polymerase chain reaction, immunoblots, immunohistochemistry, small interfering RNA, chromatin immunoprecipitation analyses, and cell transplantation into mice.
resultsIn human PDA cells, E47 activity triggers stable G0/G1 arrest, which requires the cyclin-dependent kinase inhibitor p21 and the stress response protein TP53INP1. Concurrently, E47 induces high level expression of acinar digestive enzymes and feed forward activation of the acinar maturation network regulated by the bHLH factor MIST1. Moreover, induction of E47 in human PDA cells in vitro is sufficient to inhibit tumorigenesis.
conclusionsHuman PDA cells retain a high degree of plasticity, which can be exploited to induce a quiescent acinar cell state with reduced tumorigenic potential. Moreover, bHLH activity is a critical node coordinately regulating human PDA cell growth versus cell fate.
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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.