ArticleAmerican journal of cancer research2020
Ubiquitin-like protein FAT10 promotes osteosarcoma glycolysis and growth by upregulating PFKFB3 via stabilization of EGFR.
Article in American journal of cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 22 citations in OpenAlex.
- Exploration of the mechanism by which Ubiquitin-like protein UBD promotes malignant progression of breast cancer.Medical oncology (Northwood, London, England) · 2026Article
- Exploring the role of protein homeostasis regulation in glycolysis in head and neck tumors.Human cell · 2026Review
- Multi-omics reveals FAT10 as an immunometabolic survival factor rewiring global metabolism in cancer.Cell communication and signaling : CCS · 2025Article
- The Role of Ubiquitination in Osteosarcoma Development and Therapies.Biomolecules · 2024Review
- The prognostic value of ubiquitin/ubiquitin-like-related genes along with immune cell infiltration and clinicopathological features in osteosarcoma.Journal of orthopaedic surgery and research · 2024Article
- Reprogramming of glucose metabolism: Metabolic alterations in the progression of osteosarcoma.Journal of bone oncology · 2024Review
- Article
- Structure-Based Multi-Targeted Molecular Docking and Dynamic Simulation of Soybean-Derived Isoflavone Genistin as a Potential Breast Cancer Signaling Proteins Inhibitor.Life (Basel, Switzerland) · 2023Article
- Deubiquitinating enzyme USP10 promotes osteosarcoma metastasis and epithelial-mesenchymal transition by stabilizing YAP1.Cancer medicine · 2023Article
- Deubiquitinase USP33 promotes the glycolysis and growth of osteosarcoma by modifying PFKFB3 ubiquitination and degradation.American journal of cancer research · 2023Article
- SIX4 upregulates IDH1 and metabolic reprogramming to promote osteosarcoma progression.Journal of cellular and molecular medicine · 2023Article
- A glycometabolic gene signature associating with immune infiltration and chemosensitivity and predicting the prognosis of patients with osteosarcoma.Frontiers in medicine · 2023Article
- Emerging Role of Neutrophil Extracellular Traps in Gastrointestinal Tumors: A Narrative Review.International journal of molecular sciences · 2022Review
- Mechanism and Role of Endoplasmic Reticulum Stress in Osteosarcoma.Biomolecules · 2022Review
- FAT10 promotes chemotherapeutic resistance in pancreatic cancer by inducing epithelial-mesenchymal transition via stabilization of FOXM1 expression.Cell death & disease · 2022Article
- Hyperglycemia induces miR-26-5p down-regulation to overexpress PFKFB3 and accelerate epithelial-mesenchymal transition in gastric cancer.Bioengineered · 2022Article
- The roles of glycolysis in osteosarcoma.Frontiers in pharmacology · 2022Review
- Ubiquitin D Promotes Progression of Oral Squamous Cell Carcinoma via NF-Kappa B Signaling.Molecules and cells · 2021Article
- New Insights into LINC00346 and its Role in Disease.Frontiers in cell and developmental biology · 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
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteosarcoma is a major cause of cancer-related deaths in adolescents. While it thrives in a state of malnutrition, the mechanism of metabolic stress adaptation via metabolic reprogramming is unclear. Here, we found that the level of FAT10, a ubiquitin-like protein, was significantly higher in tumors than in adjacent normal tissues. Moreover, high FAT10 levels were closely related to increased malignancy and shorter survival time in osteosarcoma patients. Multivariate analysis also showed that FAT10 overexpression was an independent predictor of poor prognosis. Functional assays indicated that FAT10 promoted osteosarcoma cell proliferation by inducing glycolysis. In addition, FAT10 knockdown reduced the level of PFKFB3, a positive regulator of glycolysis in many cancers. A positive correlation was found between FAT10 and PFKFB3 levels in osteosarcoma tissues, further indicating that FAT10 induced an increase in glycolysis and that cell growth depended on PFKFB3. Interestingly, FAT10 regulated PFKFB3 expression by directly binding to EGFR and inhibiting its ubiquitination and degradation. These results shed light on the mechanisms responsible for osteosarcoma cell survival in the malnourished tumor microenvironment. Further, the results provide insights into the role of FAT10 in the adaptation of osteosarcoma cells to metabolic stress.
Indexed as
Identifiers
32775001PMC7407346W3049736520What 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.