ArticleBioengineered2022
Fat mass and obesity associated (FTO)-mediated N6-methyladenosine modification of Krüppel-like factor 3 (KLF3) promotes osteosarcoma progression.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- Decoding osteosarcoma pathogenesis: the pivotal influence of mEpigenetics · 2026Review
- FTO-mediated m6A modification of protein disulfide-isomerase activates VEGFA-VEGFR2 to suppress programmed cell death in osteosarcoma.The Journal of pathology · 2026Article
- FTO in Bone Diseases: Functions, Mechanisms and Therapeutic Potential.Biomolecules · 2026Review
- The Multitalented Marvels: Exploring the Versatile Potential of Natural Products in Osteosarcoma Treatment.Cancer informatics · 2026Review
- Research progress on N6-methyladenosine RNA modification in osteosarcoma: functions, mechanisms, and potential clinical applications.Medical oncology (Northwood, London, England) · 2025Review
- Demethylase FTO mediates m6A modification of ENST00000619282 to promote apoptosis escape in rheumatoid arthritis and the intervention effect of Xinfeng Capsule.Frontiers in immunology · 2025Article
- FTO-mediated demethylation of MTUS1/ATIP1 promotes tumor progression in head and neck squamous cell carcinoma.BMC cancer · 2024Article
- Versatility of 14-3-3 proteins and their roles in bone and joint-related diseases.Bone research · 2024Review
- N6-Methyladenosine Methylation of mRNA in Cell Apoptosis.Molecular neurobiology · 2024Review
- Novel Insights into the Links between N6-Methyladenosine and Regulated Cell Death in Musculoskeletal Diseases.Biomolecules · 2024Review
- KLF transcription factors in bone diseases.Journal of cellular and molecular medicine · 2024Review
- Recent advances of m6A methylation in skeletal system disease.Journal of translational medicine · 2024Review
- Article
- N6-methyladenosine (m6A) modification in osteosarcoma: expression, function and interaction with noncoding RNAs - an updated review.Epigenetics · 2023Review
- Nano-Based Drug Delivery Systems: Potential Developments in the Therapy of Metastatic Osteosarcoma-A Narrative Review.Pharmaceutics · 2023Review
- Qiteng Xiaozhuo granules medicated serum inhibits excessive proliferation and promotes apoptosis of human glomerular mesangial cells by targeting fat mass and obesity associated proteins.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- Network pharmacology-based research on the effect of angelicin on osteosarcoma and the underlying mechanism.Aging · 2023Article
- Pan-cancer analysis of Krüppel-like factor 3 and its carcinogenesis in pancreatic cancer.Frontiers in immunology · 2023Article
- Molecular mechanisms of osteosarcoma metastasis and possible treatment opportunities.Frontiers in oncology · 2023Review
- Krüppel-like factors in tumors: Key regulators and therapeutic avenues.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ARSTRACTN6-methyladenosine (m6A) methylation is the most common and abundant methylation modification of eukaryotic mRNAs, which is involved in tumor initiation and progression. The study aims to explore the potential role and the regulatory mechanism of fat mass and obesity associated (FTO) in osteosarcoma (OS) progression. In this study, we detected the expressions of Krüppel-like factor 3 (KLF3) in OS cells and tissues and found that the mRNA and protein levels of KLF3 were increased in OS cells and tissues and significantly related to tumor size, metastasis, and TNM stage and poor prognosis of OS patients. FTO promoted the proliferation and invasion and suppressed apoptosis of OS cells through cell experiments in vitro. Further mechanism dissection revealed that FTO and YTHDF2 enforced the decay of KLF3 mRNA and decreased its expression. FTO-mediated mRNA demethylation inhibited KLF3 expression in the YTHDF2-dependent manner. Moreover, KLF3 overexpression abrogated FTO-induced oncogenic effects on the proliferation and invasion of OS cells. Overall, our findings showed that FTO-mediated m6A modification of KLF3 promoted OS progression, which may provide a therapeutic target for 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 Socratic graph.