ArticleThe EMBO journal2023
YAP/BRD4-controlled ROR1 promotes tumor-initiating cells and hyperproliferation in pancreatic cancer.
Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- BRD4: From molecular understanding to therapeutics development.Molecular cell · 2026Review
- Quantum Reactivity-Guided Optimization of ATP-Competitive Ligands through Multiscale Simulation.ACS physical chemistry Au · 2026Article
- Targeting ROR1 with humanized antibody drug conjugates and cytokine fusion proteins for cancer therapy.iScience · 2026Article
- ROR1 protein: a pseudokinase at the crossroads of cancer progression and therapy.Molecular biology reports · 2026Review
- Plasma Proteomic Profiling Reveals Distinct Signatures of Chest CT Phenotypes in Sarcoidosis.Research square · 2025Article
- The Role of Receptor Tyrosine Kinase-like Orphan Receptor 1 (ROR1) in Cancer Stem Cell Signaling.International journal of molecular sciences · 2025Review
- Single-Cell Analysis Clarifies Pathological Heterogeneity in Tenosynovial Giant Cell Tumor and Identifies Biomarkers for Predicting Disease Recurrence.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Plasma Proteomic Profiling Reveals Distinct Signatures of Chest CT Phenotypes in Sarcoidosis.bioRxiv : the preprint server for biology · 2025Article
- VCPIP1 facilitates pancreatic adenocarcinoma progression via Hippo/YAP signaling.Cell death & disease · 2025Article
- Unveiling CTRB2, RSPO3, KLOTB, and ROR1 as obesity-pancreatic disease association proteins: a comprehensive Mendelian randomization study.Gastroenterology report · 2025Article
- Unlocking the potential: advancements and future horizons in ROR1-targeted cancer therapies.Science China. Life sciences · 2024Review
- Extracellular vesicles miR-31-5p promotes pancreatic cancer chemoresistance via regulating LATS2-Hippo pathway and promoting SPARC secretion from pancreatic stellate cells.Journal of extracellular vesicles · 2024Article
- Variant Transcript of ROR1 ENST00000545203 Does Not Encode ROR1 Protein.Biomedicines · 2024Article
- A Review of the Bromodomain and Extraterminal Domain Epigenetic Reader Proteins: Function on Virus Infection and Cancer.Viruses · 2024Review
- Receptor tyrosine kinase-like orphan receptor 1: A novel antitumor target in gastrointestinal cancers.World journal of clinical oncology · 2024Review
- Inhibition of Bromodomain Proteins Enhances Oncolytic HAdVC5 Replication and Efficacy in Pancreatic Ductal Adenocarcinoma (PDAC) Models.International journal of molecular sciences · 2024Article
- ROR2 regulates cellular plasticity in pancreatic neoplasia and adenocarcinoma.bioRxiv : the preprint server for biology · 2024Article
- Exosomal ROR1 in peritoneal fluid identifies peritoneal disseminated PDAC and is associated with poor survival.Frontiers in immunology · 2024Article
- The potential of BRD4 inhibition in tumour mechanosignaling.Journal of cellular and molecular medicine · 2023Article
- Epigenetic control of pancreatic cancer metastasis.Cancer metastasis reviews · 2023Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor-initiating cells are major drivers of chemoresistance and attractive targets for cancer therapy, however, their identity in human pancreatic ductal adenocarcinoma (PDAC) and the key molecules underlying their traits remain poorly understood. Here, we show that a cellular subpopulation with partial epithelial-mesenchymal transition (EMT)-like signature marked by high expression of receptor tyrosine kinase-like orphan receptor 1 (ROR1) is the origin of heterogeneous tumor cells in PDAC. We demonstrate that ROR1 depletion suppresses tumor growth, recurrence after chemotherapy, and metastasis. Mechanistically, ROR1 induces the expression of Aurora kinase B (AURKB) by activating E2F through c-Myc to enhance PDAC proliferation. Furthermore, epigenomic analyses reveal that ROR1 is transcriptionally dependent on YAP/BRD4 binding at the enhancer region, and targeting this pathway reduces ROR1 expression and prevents PDAC growth. Collectively, our findings reveal a critical role for ROR1high cells as tumor-initiating cells and the functional importance of ROR1 in PDAC progression, thereby highlighting its therapeutic targetability.
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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.