ArticleCancer letters2011
Notch-1 induces epithelial-mesenchymal transition consistent with cancer stem cell phenotype in pancreatic cancer cells.
Article in Cancer letters, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 168 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.
The trial behind it
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
168 citing papers in PubMed, 280 citations in OpenAlex.
- The effect of aspirin on circulating tumor cells in metastatic colorectal and breast cancer patients: a phase II trial study.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018Trial
- Oncolytic viral therapy as a novel potential solution for treatment of pancreatic cancer.Gastroenterology and hepatology from bed to bench · 2025Review
- Everything you ever wanted to know about cancer stem cells in neuroendocrine neoplasms but were afraid to ask.Endocrine oncology (Bristol, England) · 2024Review
- Pancreatic cancer stemness: dynamic status in malignant progression.Journal of experimental & clinical cancer research : CR · 2023Review
- Review
- Cigarette Smoke Impairs Airway Epithelial Wound Repair: Role of Modulation of Epithelial-Mesenchymal Transition Processes and Notch-1 Signaling.Antioxidants (Basel, Switzerland) · 2022Article
- Pancreatic cancer cell-derived exosomes induce epithelial-mesenchymal transition in human pancreatic cancer cells themselves partially via transforming growth factor β1.Medical molecular morphology · 2022Article
- Global research hotspots and trends of the Notch signaling pathway in the field of cancer: a bibliometric study.American journal of translational research · 2022Article
- Antitumor Effect of Pseudolaric Acid B Involving Regulation of Notch1/Akt Signaling Response in Human Hepatoma Cell In Vitro.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- An Extensive Review on Preclinical and Clinical Trials of Oncolytic Viruses Therapy for Pancreatic Cancer.Frontiers in oncology · 2022Review
- Complementary effects of Orthosiphon stamineus standardized ethanolic extract and rosmarinic acid in combination with gemcitabine on pancreatic cancer.Biomedical journal · 2021Article
- Review
- FZD2 promotes TGF-β-induced epithelial-to-mesenchymal transition in breast cancer via activating notch signaling pathway.Cancer cell international · 2021Article
- The Interaction of the Senescent and Adjacent Breast Cancer Cells Promotes the Metastasis of Heterogeneous Breast Cancer Cells through Notch Signaling.International journal of molecular sciences · 2021Article
- Upregulation of KLK8 Predicts Poor Prognosis in Pancreatic Cancer.Frontiers in oncology · 2021Article
- Isolation and evaluation of cardenolides from Lansium domesticum as Notch inhibitors.Journal of natural medicines · 2020Article
- Mechanism of Notch1‑saRNA‑1480 reversing androgen sensitivity in human metastatic castration‑resistant prostate cancer.International journal of molecular medicine · 2020Article
- Effect of miR‑449a‑mediated Notch signaling pathway on the proliferation, apoptosis and invasion of papillary thyroid carcinoma cells.Oncology reports · 2020Article
- MiRNA and LncRNA as Potential Biomarkers in Triple-Negative Breast Cancer: A Review.Frontiers in oncology · 2020Review
- Construction and Validation of a Robust Cancer Stem Cell-Associated Gene Set-Based Signature to Predict Early Biochemical Recurrence in Prostate Cancer.Disease markers · 2020Article
108 more citing papers are in PubMed but not listed here.
Corrections and comments
- Retraction · 2018-03-29Falsification/Fabrication of Data · Investigation by Company/Institution · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author ·
- Retracted
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Activation of Notch-1 is known to be associated with the development and progression of human malignancies including pancreatic cancer. Emerging evidence suggest that the acquisition of epithelial-mesenchymal transition (EMT) phenotype and induction of cancer stem cell (CSC) or cancer stem-like cell phenotype are interrelated and contributes to tumor recurrence and drug resistance. The molecular mechanism(s) by which Notch-1 contributes to the acquisition of EMT phenotype and CSC self-renewal capacity has not been fully elucidated. Here we show that forced over-expression of Notch-1 leads to increased cell growth, clonogenicity, migration and invasion of AsPC-1 cells. Moreover, over-expression of Notch-1 led to the induction of EMT phenotype by activation of mesenchymal cell markers such as ZEB1, CD44, EpCAM, and Hes-1. Here we also report, for the first time, that over-expression of Notch-1 leads to increased expression of miR-21, and decreased expression of miR-200b, miR-200c, let-7a, let-7b, and let-7c. Re-expression of miR-200b led to decreased expression of ZEB1, and vimentin, and increased expression of E-cadherin. Over-expression of Notch-1 also increased the formation of pancreatospheres consistent with expression of CSC surface markers CD44 and EpCAM. Finally, we found that genistein, a known natural anti-tumor agent inhibited cell growth, clonogenicity, migration, invasion, EMT phenotype, formation of pancreatospheres and expression of CD44 and EpCAM. These results suggest that the activation of Notch-1 signaling contributes to the acquisition of EMT phenotype, which is in part mediated through the regulation of miR-200b and CSC self-renewal capacity, and these processes could be attenuated by genistein treatment.
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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.