ArticleJournal of cellular and molecular medicine2025
TRIM47 Facilitates Osteosarcoma Progression via Destabilising FBP1 and Thus Activation of Wnt/β-Catenin Pathway.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- TRIM47 promotes cell viability, cell cycle progression, metabolic reprogramming, and inhibits apoptosis of glioma via the NF-κB signaling pathway.Translational cancer research · 2026Article
- TRIM47: molecular characteristics, disease-related mechanisms, and clinical translational value.Frontiers in immunology · 2026Review
- An Epithelial-Mesenchymal Transition-Driven Transcriptional Index Stratifies Immunosuppression and Therapeutic Resistance in Bone Malignancies.International journal of genomics · 2026Article
- TRIM47 Facilitates Osteosarcoma Progression via Destabilising FBP1 and Thus Activation of Wnt/β-Catenin Pathway.Journal of cellular and molecular medicine · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
Osteosarcoma is a malignant bone tumour with a high rate of disability and mortality in adolescents. Tripartite motif containing 47 (TRIM47) upregulation contributed greatly to carcinogenesis and progression in several tumours, while its role in osteosarcoma (OS) is still unclear and needs further investigation. In this study, we first evidenced that TRIM47 was frequently upregulated in osteosarcoma tissues and cell lines, and the higher TRIM47 expression predicted poor outcomes for osteosarcoma patients. Moreover, TRIM47 depletion impeded cell proliferation, migration, and invasion of osteosarcoma cells, while TRIM47 overexpression elicited opposite effects. Mechanistically, TRIM47 interacted with and accelerated the degradation of fructose 1, 6-bisphosphatase 1 (FBP1) by inducing its ubiquitination, subsequently activating the Wnt/β-catenin signalling pathway. Furthermore, knockdown of FBP1 reversed the functions of TRIM47 depletion in OS cells. More notably, our in vivo assays showed that loss of TRIM47 slowed the growth rate of osteosarcoma xenograft tumours. Overall, our data indicated that TRIM47 facilitates OS progression by promoting proteasomal degradation of FBP1, thereby activating the Wnt/β-catenin pathway, which clarified that targeting the TRIM47-FBP1-β-catenin axis could be a promising approach for treating OS.
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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.