ArticleCancer letters2018
Inhibition of FASN and ERα signalling during hyperglycaemia-induced matrix-specific EMT promotes breast cancer cell invasion via a caveolin-1-dependent mechanism.
Article in Cancer letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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
39 citing papers in PubMed, 54 citations in OpenAlex.
- Hyperglycaemia-Induced Metabolic Stress Promotes EMT-Driven Therapeutic Resistance in Cancer: Evidence of a Deleterious Feed-Forward Cycle.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Targeting caveolin-1: dual challenges in tumor immunity and drug therapy strategies.Cancer cell international · 2026Review
- EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025Review
- Orchestrating movement: the role of Caveolin-1 in migration and metastasis.Molecular cancer · 2025Review
- FASN inhibits ferroptosis in breast cancer via USP5 palmitoylation-dependent regulation of GPX4 deubiquitination.Journal of experimental & clinical cancer research : CR · 2025Article
- Lipid metabolic reprograming: the unsung hero in breast cancer progression and tumor microenvironment.Molecular cancer · 2025Review
- Hyaluronic Acid Influences Amino Acid Metabolism via Differential L-Type Amino Acid Transporter 1 Expression in the U87-Malignant Glioma Cell Line.Advanced nanobiomed research · 2024Article
- Influence of Type 2 Diabetes and Adipose Tissue Dysfunction on Breast Cancer and Potential Benefits from Nutraceuticals Inducible in Microalgae.Nutrients · 2024Review
- Tobacco-induced hyperglycemia promotes lung cancer progression via cancer cell-macrophage interaction through paracrine IGF2/IR/NPM1-driven PD-L1 expression.Nature communications · 2024Article
- Fatty acid synthase (FASN) signalome: A molecular guide for precision oncology.Molecular oncology · 2024Article
- Diabetes-associated breast cancer is molecularly distinct and shows a DNA damage repair deficiency.JCI insight · 2023Article
- Role of EGFR and FASN in breast cancer progression.Journal of cell communication and signaling · 2023Review
- Single-cell transcriptome analysis indicates fatty acid metabolism-mediated metastasis and immunosuppression in male breast cancer.Nature communications · 2023Article
- Role of Caveolae family-related proteins in the development of breast cancer.Frontiers in molecular biosciences · 2023Review
- microRNA-26b inhibits growth and cellular invasion of ovarian cancer cells by targeting estrogen receptor α.3 Biotech · 2022Article
- Dihydrotanshinone I Enhances Cell Adhesion and Inhibits Cell Migration in Osteosarcoma U-2 OS Cells through CD44 and Chemokine Signaling.Molecules (Basel, Switzerland) · 2022Article
- Metabolomics and EMT Markers of Breast Cancer: A Crosstalk and Future Perspective.Pathophysiology : the official journal of the International Society for Pathophysiology · 2022Review
- The crosstalk within the breast tumor microenvironment in type II diabetes: Implications for cancer disparities.Frontiers in endocrinology · 2022Review
- Exploring the molecular targets and mechanisms of [10]-Gingerol for treating triple-negative breast cancer using bioinformatics approaches, molecular docking, andTranslational cancer research · 2021Article
- Research progress on FASN and MGLL in the regulation of abnormal lipid metabolism and the relationship between tumor invasion and metastasis.Frontiers of medicine · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Since disturbed metabolic conditions such as obesity and diabetes can be critical determinants of breast cancer progression and therapeutic failure, we aimed to determine the mechanism responsible for their pro-oncogenic effects. Using non-invasive, epithelial-like ERα-positive MCF-7 and T47D human breast cancer cells we found that hyperglycaemia induced epithelial to mesenchymal transition (EMT), a key programme responsible for the development of metastatic disease. This was demonstrated by loss of the epithelial marker E-cadherin together with increases in mesenchymal markers such as vimentin, fibronectin and the transcription factor SLUG, together with an enhancement of cell growth and invasion. These phenotypic changes were only observed with cells grown on fibronectin and not with those plated on collagen. Analyzing metabolic parameters, we found that hyperglycaemia-induced, matrix-specific EMT promoted the Warburg effect by upregulating glucose uptake, lactate release and specific glycolytic enzymes and transporters. We showed that silencing of fatty acid synthase (FASN) and the downstream ERα, which we showed previously to mediate hyperglycaemia-induced chemoresistance in these cells, resulted in suppression of cell growth: however, this also resulted in a dramatic enhancement of cell invasion and SLUG mRNA levels via a novel caveolin-1-dependent mechanism.
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.