ArticleOncology letters2017
Changes in mitochondrial function during EMT induced by TGFβ-1 in pancreatic cancer.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Hafnium-Oxide Based Nanoplatform with Tumor Microenvironment Responsive Drug Release for Enhanced Radio-Chemotherapy.International journal of nanomedicine · 2026Article
- A morphology-based machine learning model for scoring epithelial-mesenchymal plasticity using organelle dynamics.Communications biology · 2025Article
- Spatiotemporal Heterogeneity of Tumor Glucose Metabolism Reprogramming: From Single-Cell Mechanisms to Precision Interventions.International journal of molecular sciences · 2025Review
- Broadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transition.Cell communication and signaling : CCS · 2025Review
- The Effect of Ionising Radiation on the Properties of Tumour-Derived Exosomes and Their Ability to Modify the Biology of Non-Irradiated Breast Cancer Cells-An In Vitro Study.International journal of molecular sciences · 2025Article
- EPRS1-mediated fibroblast activation and mitochondrial dysfunction promote kidney fibrosis.Experimental & molecular medicine · 2024Article
- Biological and Clinical Impacts of Glucose Metabolism in Pancreatic Ductal Adenocarcinoma.Cancers · 2023Review
- TGFβ Signaling in the Pancreatic Tumor Microenvironment.Cancers · 2021Review
- Quantitative Proteomic Analysis in Alveolar Type II Cells Reveals the Different Capacities of RAS and TGF-β to Induce Epithelial-Mesenchymal Transition.Frontiers in molecular biosciences · 2021Article
- EMT signaling: potential contribution of CRISPR/Cas gene editing.Cellular and molecular life sciences : CMLS · 2020Review
- TGFβ-dependent mitochondrial biogenesis is activated during definitive endoderm differentiation.In vitro cellular & developmental biology. Animal · 2020Article
- The enhancement of glycolysis regulates pancreatic cancer metastasis.Cellular and molecular life sciences : CMLS · 2020Review
- Intrinsic and Extrinsic Modulators of the Epithelial to Mesenchymal Transition: Driving the Fate of Tumor Microenvironment.Frontiers in oncology · 2020Review
- Redox Imbalance in Idiopathic Pulmonary Fibrosis: A Role for Oxidant Cross-Talk Between NADPH Oxidase Enzymes and Mitochondria.Antioxidants & redox signaling · 2019Review
- Endothelial to Mesenchymal Transition in Cardiovascular Disease: JACC State-of-the-Art Review.Journal of the American College of Cardiology · 2019Review
- Correlation between S100A11 and the TGF-βMolecular and cellular biochemistry · 2019Article
- Elucidating the Metabolic Plasticity of Cancer: Mitochondrial Reprogramming and Hybrid Metabolic States.Cells · 2018Review
- Functional Isolation of Tumor-Initiating Cells using Microfluidic-Based Migration Identifies Phosphatidylserine Decarboxylase as a Key Regulator.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is linked to cancer. Differences in the number, morphology and function of mitochondria have been observed between normal cells and cancer cells. However, changes in mitochondrial function during epithelial-mesenchymal transition (EMT) in pancreatic cancer are less known. In the present study, the cultured human pancreatic cancer cell line Panc-1 was treated with transforming growth factor (TGF)β-1. Mitochondrial functions following TGFβ-1 exposure in pancreatic cancer were investigated. It was noticed that TGFβ-1 treatment induces morphologic changes and a shift from epithelial to mesenchymal phenotype in pancreatic cancer. Furthermore, increased mitochondrial mass was detected in pancreatic cancer following TGFβ-1 treatment. Besides, the production of reactive oxygen species in TGFβ-1-treated pancreatic cancer cells significantly increased compared with the control cells. Our results indicate that the phenomenon of EMT in pancreatic cancer has an association with mitochondrial dysfunction. Mitochondrial dysfunction may be a cause of EMT in pancreatic cancer, which leads to heterogeneity in pancreatic cancer, and may be a potential therapeutic target in the future.
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