ArticleJournal of cellular biochemistry2011
Over-expression of FoxM1 leads to epithelial-mesenchymal transition and cancer stem cell phenotype in pancreatic cancer cells.
Article in Journal of cellular biochemistry, 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 It has been retracted, and should not be counted.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 123 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
123 citing papers in PubMed, 1 synthesis or guideline pooled it, 209 citations in OpenAlex.
- Prognostic Value of FOXM1 in Patients with Malignant Solid Tumor: A Meta-Analysis and System Review.Disease markers · 2015Pooled it
- Leveraging the molecular insights and therapeutic potential of diet-derived-flavonoids against pancreatic ductal adenocarcinoma.Frontiers in pharmacology · 2026Review
- Unraveling the molecular landscape of pancreatic cancer: a systems biology approach to identify therapeutic targets.Discover oncology · 2025Article
- The conformation of FOXM1 homodimers in vivo is crucial for regulating transcriptional activities.Nucleic acids research · 2024Article
- Vitamin D and Its Receptors in Cervical Cancer.Journal of Cancer · 2024Review
- Role of Fork-Head Box Genes in Breast Cancer: From Drug Resistance to Therapeutic Targets.Biomedicines · 2023Review
- Landscape of NcRNAs involved in drug resistance of breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Single-Cell Transcriptomics Unveils the Dedifferentiation Mechanism of Lung Adenocarcinoma Stem Cells.International journal of molecular sciences · 2022Article
- Post-Translational Modification of ZEB Family Members in Cancer Progression.International journal of molecular sciences · 2022Review
- The Molecular and Cellular Strategies of Glioblastoma and Non-Small-Cell Lung Cancer Cells Conferring Radioresistance.International journal of molecular sciences · 2022Review
- Effects of thiostrepton alone or in combination with selumetinib on triple-negative breast cancer metastasis.Molecular biology reports · 2022Article
- Laminarin Attenuates ROS-Mediated Cell Migration and Invasiveness through Mitochondrial Dysfunction in Pancreatic Cancer Cells.Antioxidants (Basel, Switzerland) · 2022Article
- A lignan from Alnus japonica inhibits glioblastoma tumorspheres by suppression of FOXM1.Scientific reports · 2022Article
- Genistein promotes apoptosis of lung cancer cells through the IMPDH2/AKT1 pathway.American journal of translational research · 2022Article
- Genistein inhibits lung cancer cell stem-like characteristics by modulating MnSOD and FoxM1 expression.Oncology letters · 2020Article
- Circ-MMP2 (circ-0039411) induced by FOXM1 promotes the proliferation and migration of lung adenocarcinoma cells in vitro and in vivo.Cell death & disease · 2020Article
- Aberrations in Notch-Hedgehog signalling reveal cancer stem cells harbouring conserved oncogenic properties associated with hypoxia and immunoevasion.British journal of cancer · 2019Article
- Dynamically decreased miR-671-5p expression is associated with oncogenic transformation and radiochemoresistance in breast cancer.Breast cancer research : BCR · 2019Article
- FOXM1 is a novel predictor of recurrence in patients with oral squamous cell carcinoma associated with an increase in epithelial‑mesenchymal transition.Molecular medicine reports · 2019Article
- Hypoxia-driven paracrine osteopontin/integrin αvβ3 signaling promotes pancreatic cancer cell epithelial-mesenchymal transition and cancer stem cell-like properties by modulating forkhead box protein M1.Molecular oncology · 2019Article
63 more citing papers are in PubMed but not listed here.
Corrections and comments
- Retraction · 2016-08-01Duplication of/in Image · Investigation by Company/Institution · Manipulation of Images · Misconduct - Official Investigation(s) and/or Finding(s) · · Wayne State University investigated Fazlul Sarkar
- Retracted
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
FoxM1 is known to play important role in the development and progression of many malignancies including pancreatic cancer. Studies have shown that the acquisition of epithelial-to-mesenchymal transition (EMT) phenotype and induction of cancer stem cell (CSC) or cancer stem-like cell phenotypes are highly inter-related, and contributes to drug resistance, tumor recurrence, and metastasis. The molecular mechanism(s) by which FoxM1 contributes to the acquisition of EMT phenotype and induction of CSC self-renewal capacity is poorly understood. Therefore, we established FoxM1 over-expressing pancreatic cancer (AsPC-1) cells, which showed increased cell growth, clonogenicity, and cell migration. Moreover, over-expression of FoxM1 led to the acquisition of EMT phenotype by activation of mesenchymal cell markers, ZEB1, ZEB2, Snail2, E-cadherin, and vimentin, which is consistent with increased sphere-forming (pancreatospheres) capacity and expression of CSC surface markers (CD44 and EpCAM). We also found that over-expression of FoxM1 led to decreased expression of miRNAs (let-7a, let-7b, let-7c, miR-200b, and miR-200c); however, re-expression of miR-200b inhibited the expression of ZEB1, ZEB2, vimentin as well as FoxM1, and induced the expression of E-cadherin, leading to the reversal of EMT phenotype. Finally, we found that genistein, a natural chemo-preventive agent, inhibited cell growth, clonogenicity, cell migration and invasion, EMT phenotype, and formation of pancreatospheres consistent with reduced expression of CD44 and EpCAM. These results suggest, for the first time, that FoxM1 over-expression is responsible for the acquisition of EMT and CSC phenotype, which is in part mediated through the regulation of miR-200b and these processes, could be easily attenuated by genistein.
Indexed as
Identifiers
What OpenQuestion holds
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.