ArticleJournal of cell science2017
The Aurora-A-Twist1 axis promotes highly aggressive phenotypes in pancreatic carcinoma.
Article in Journal of cell science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
49 citing papers in PubMed, 65 citations in OpenAlex.
- Machine Learning-Based Identification of Survival-Associated CpG Biomarkers in Pancreatic Ductal Adenocarcinoma.Journal of precision medicine (Amsterdam, Netherlands) · 2026Article
- Pancreatic cancer EMT‑targeted therapy: Molecular mechanisms and clinical translation (Review).International journal of oncology · 2026Review
- Splice-switching ASOs targeting the AURKA 5' UTR collapse an SRSF1-AURKA-MYC oncogenic circuit in pancreatic cancer.Molecular cell · 2026Article
- Identification of ferroptosis-related signature predicting prognosis and therapeutic responses in pancreatic cancer.Scientific reports · 2025Article
- The significant others of aurora kinase a in cancer: combination is the key.Biomarker research · 2024Review
- PFDN4 as a Prognostic Marker Was Associated with Chemotherapy Resistance through CREBP1/AURKA Pathway in Triple-Negative Breast Cancer.International journal of molecular sciences · 2024Article
- Recent Updates on Oncogenic Signaling of Aurora Kinases in Chemosensitive, Chemoresistant Cancers: Novel Medicinal Chemistry Approaches for Targeting Aurora Kinases.Current medicinal chemistry · 2024Review
- Article
- LncRNA TIALD contributes to hepatocellular carcinoma metastasis via inducing AURKA lysosomal degradation.Cell death discovery · 2023Article
- Role of pelitinib in the regulation of migration and invasion of hepatocellular carcinoma cells via inhibition of Twist1.BMC cancer · 2023Article
- TWIST1 is a prognostic factor for neoadjuvant chemotherapy for patients with resectable pancreatic cancer: a preliminary study.Surgery today · 2023Article
- Article
- Aurora kinase a inhibitor MLN8237 suppresses pancreatic cancer growth.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2022Article
- Mitotic protein kinase-driven crosstalk of machineries for mitosis and metastasis.Experimental & molecular medicine · 2022Review
- The Role of Feedback Loops in Targeted Therapy for Pancreatic Cancer.Frontiers in oncology · 2022Review
- Reciprocal deregulation of NKX3.1 and AURKA axis in castration-resistant prostate cancer and NEPC models.Journal of biomedical science · 2021Article
- ISL1 promoted tumorigenesis and EMT via Aurora kinase A-induced activation of PI3K/AKT signaling pathway in neuroblastoma.Cell death & disease · 2021Article
- Article
- Aurora kinase A, a synthetic lethal target for precision cancer medicine.Experimental & molecular medicine · 2021Review
- The Post-Translational Regulation of Epithelial-Mesenchymal Transition-Inducing Transcription Factors in Cancer Metastasis.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
We uncovered a crucial role for the Aurora kinase A (AURKA)-Twist1 axis in promoting epithelial-to-mesenchymal transition (EMT) and chemoresistance in pancreatic cancer. Twist1 is the first EMT-specific target of AURKA that was identified using an innovative screen. AURKA phosphorylates Twist1 at three sites, which results in its multifaceted regulation - AURKA inhibits its ubiquitylation, increases its transcriptional activity and favors its homodimerization. Twist1 reciprocates and prevents AURKA degradation, thereby triggering a feedback loop. Ablation of either AURKA or Twist1 completely inhibits EMT, highlighting both proteins as central players in EMT progression. Phosphorylation-dead Twist1 serves as a dominant-negative and fully reverses the EMT phenotype induced by Twist1, underscoring the crucial role of AURKA-mediated phosphorylation in mediating Twist1-induced malignancy. Likewise, Twist1-overexpressing BxPC3 cells formed large tumors
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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.