ArticleJournal of cellular and molecular medicine2020
Positive feedback in Cav-1-ROS signalling in PSCs mediates metabolic coupling between PSCs and tumour cells.
Article in Journal of cellular and molecular medicine, 2020. 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 It has been retracted, and should not be counted.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 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Prognostic value of glycolysis markers in pancreatic cancer: A systematic review and meta-analysis.Frontiers in oncology · 2022Pooled it
- PFKP in malignant tumors: bridging metabolic reprogramming, post-translational modifications, and the immunosuppressive microenvironment.Frontiers in cell and developmental biology · 2026Review
- RETRACTION: Positive Feedback in Cav-1-ROS Signalling in PSCs Mediates Metabolic Coupling between PSCs and Tumour Cells.Journal of cellular and molecular medicine · 2025Article
- Extracellular Vesicle-Packaged Linc-ZNF25-1 from Pancreatic Cancer Cell Promotes Pancreatic Stellate Cell Uptake of Asparagine to Advance Chemoresistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The anti-neoplastic effects of metformin modulate the acquired phenotype of fibroblast cells in the breast cancer-normal fibroblast co-culture system.Oncology research · 2024Article
- Pancreatic cancer and fibrosis: Targeting metabolic reprogramming and crosstalk of cancer-associated fibroblasts in the tumor microenvironment.Frontiers in immunology · 2023Review
- Epigallocatechin‑3‑gallate hinders metabolic coupling to suppress colorectal cancer malignancy through targeting aerobic glycolysis in cancer‑associated fibroblasts.International journal of oncology · 2022Article
- The Role of Feedback Loops in Targeted Therapy for Pancreatic Cancer.Frontiers in oncology · 2022Review
- Pancreatic Stellate Cells and Metabolic Alteration: Physiology and Pathophysiology.Frontiers in physiology · 2022Review
- Role of reactive oxygen species in tumors based on the 'seed and soil' theory: A complex interaction (Review).Oncology reports · 2021Review
- Targeted Inhibition of HK-II Reversed the Warburg Effect to Improve the Radiosensitivity of Laryngeal Carcinoma.Cancer management and research · 2021Article
- Caveolin-1 Regulates Cellular Metabolism: A Potential Therapeutic Target in Kidney Disease.Frontiers in pharmacology · 2021Review
- Integrated Bioinformatic Analysis of the Expression and Prognosis of Caveolae-Related Genes in Human Breast Cancer.Frontiers in oncology · 2021Article
- Caveolin-1 Alleviates Acetaminophen-Induced Fat Accumulation in Non-Alcoholic Fatty Liver Disease by Enhancing Hepatic Antioxidant AbilityFrontiers in pharmacology · 2021Article
- Targets (Metabolic Mediators) of Therapeutic Importance in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2020Review
- Positive feedback in Cav-1-ROS signalling in PSCs mediates metabolic coupling between PSCs and tumour cells.Journal of cellular and molecular medicine · 2020Article
- The Role of Stellate Cells in Pancreatic Ductal Adenocarcinoma: Targeting Perspectives.Frontiers in oncology · 2020Review
Corrections and comments
- Retracted
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caveolin-1 (Cav-1) is the principal structural component of caveolae, and its dysregulation occurs in cancer. However, the role of Cav-1 in pancreatic cancer (PDAC) tumorigenesis and metabolism is largely unknown. In this study, we aimed to investigate the effect of pancreatic stellate cell (PSC) Cav-1 on PDAC metabolism and aggression. We found that Cav-1 is expressed at low levels in PDAC stroma and that the loss of stromal Cav-1 is associated with poor survival. In PSCs, knockdown of Cav-1 promoted the production of reactive oxygen species (ROS), while ROS production further reduced the expression of Cav-1. Positive feedback occurs in Cav-1-ROS signalling in PSCs, which promotes PDAC growth and induces stroma-tumour metabolic coupling in PDAC. In PSCs, positive feedback in Cav-1-ROS signalling induced a shift in energy metabolism to glycolysis, with up-regulated expression of glycolytic enzymes (hexokinase 2 (HK-2), 6-phosphofructokinase (PFKP) and pyruvate kinase isozyme type M2 (PKM2)) and transporter (Glut1) expression and down-regulated expression of oxidative phosphorylation (OXPHOS) enzymes (translocase of outer mitochondrial membrane 20 (TOMM20) and NAD(P)H dehydrogenase [quinone] 1 (NQO1)). These events resulted in high levels of glycolysis products such as lactate, which was secreted by up-regulated monocarboxylate transporter 4 (MCT4) in PSCs. Simultaneously, PDAC cells took up these glycolysis products (lactate) through up-regulated MCT1 to undergo OXPHOS, with down-regulated expression of glycolytic enzymes (HK-2, PFKP and PKM2) and up-regulated expression of OXPHOS enzymes (TOMM20 and NQO1). Interrupting the metabolic coupling between the stroma and tumour cells may be an effective method for tumour therapy.
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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.