ALKBH5-mediated m6A demethylation of HS3ST3B1-IT1 prevents osteoarthritis progression

Tang, Yuting; Liu, Yang; Zhu, Xiaoshu; Chen, Yanlin; Jiang, Xinluan; Ding, Siyang; Zheng, Que; Zhang, Ming; Yang, Jiashu; Ma, Yunfei; Xing, Mengying; Zhang, Zongyu; Ding, Huimin; Jin, Yucui; Ma, Changyan

doi:10.1016/j.isci.2023.107838

Cited by 3 publications

(2 citation statements)

References 47 publications

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“…Increasing evidences have shown that METTL3, WTAP, FTO and ALKBH5 are aberrantly expressed in OA chondrocytes and involved in OA pathogenesis by regulating chondrocyte proliferation, apoptosis, extracellular matrix (ECM) degradation through related signal pathways [ 69 , 72 , 80 , 84 ]. For example, Lin et al have revealed that WTAP-mediated miR-92b-5p/TIMP4 axis plays crucial role in OA development.…”

Section: M6a and Skeletal System Diseasementioning

confidence: 99%

“…Moreover, Ren et al found that METTL3 overexpression increased the LINC0068 level in OA, which repressed chondrocyte proliferation and accelerated ECM degradation [ 76 ]. Conversely, ALKBH5-mediated upregulation of HS3ST3B1-IT1 suppresses OA progression [ 84 ]. What’s more, Yang et al showed that FTO suppressed the expression of AC008, which promoted chondrocyte apoptosis and ECM degradation in OA [ 83 ].…”

Section: M6a and Skeletal System Diseasementioning

confidence: 99%

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Recent advances of m6A methylation in skeletal system disease

Liang,

Yi,

Liu

et al. 2024

J Transl Med

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Skeletal system disease (SSD) is defined as a class of chronic disorders of skeletal system with poor prognosis and causes heavy economic burden. m6A, methylation at the N6 position of adenosine in RNA, is a reversible and dynamic modification in posttranscriptional mRNA. Evidences suggest that m6A modifications play a crucial role in regulating biological processes of all kinds of diseases, such as malignancy. Recently studies have revealed that as the most abundant epigentic modification, m6A is involved in the progression of SSD. However, the function of m6A modification in SSD is not fully illustrated. Therefore, make clear the relationship between m6A modification and SSD pathogenesis might provide novel sights for prevention and targeted treatment of SSD. This article will summarize the recent advances of m6A regulation in the biological processes of SSD, including osteoporosis, osteosarcoma, rheumatoid arthritis and osteoarthritis, and discuss the potential clinical value, research challenge and future prospect of m6A modification in SSD.

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Section: M6a and Skeletal System Diseasementioning

confidence: 99%

Section: M6a and Skeletal System Diseasementioning

confidence: 99%

Recent advances of m6A methylation in skeletal system disease

Liang,

Yi,

Liu

et al. 2024

J Transl Med

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Transcriptome‐wide RNA m6A methylation profiles in an endemic osteoarthropathy, Kashin‐Beck disease

Zhang,

Yang,

Deng

et al. 2024

J Cellular Molecular Medi

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Kashin‐Beck disease (KBD) is a chronic degenerative, disabling disease of the bones and joints and its exact aetiology and pathogenesis remain uncertain. This study is to investigate the role of m6A modification in the pathogenesis of KBD. Combined analysis of m6A MeRIP‐Seq and RNA‐Seq were used to analyse human peripheral blood samples from three KBD patients and three normal controls (NC). Bioinformatic methods were used to analyse m6A‐modified differential genes and RT‐qPCR was performed to validate the mRNA expression of several KBD‐related genes. The results indicated that the total of 16,811 genes were modified by m6A in KBD group, of which 4882 genes were differential genes. A large number of differential genes were associated with regulation of transcription, signal transduction and protein binding. KEGG analysis showed that m6A‐enriched genes participated the pathways of Vitamin B6 metabolism, endocytosis and Rap 1 signalling pathway. There was a positive association between m6A abundance and levels of gene expression, that there were 6 hypermethylated and upregulated genes (hyper‐up), 23 hypomethylated and downregulated genes (hypo‐down) in KBD group compared with NC. In addition, the mRNA expression of levels of MMP8, IL32 and GPX1 were verified and the protein–protein interaction networks of these key factors were constructed. Our study showed that m6A modifications may play a vital role in modulating gene expression, which represents a new clue to reveal the pathogenesis of KBD.

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Novel Insights into the Links between N6-Methyladenosine and Regulated Cell Death in Musculoskeletal Diseases

Han,

Wang,

Yang

et al. 2024

Biomolecules

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Musculoskeletal diseases (MSDs), including osteoarthritis (OA), osteosarcoma (OS), multiple myeloma (MM), intervertebral disc degeneration (IDD), osteoporosis (OP), and rheumatoid arthritis (RA), present noteworthy obstacles associated with pain, disability, and impaired quality of life on a global scale. In recent years, it has become increasingly apparent that N6-methyladenosine (m6A) is a key regulator in the expression of genes in a multitude of biological processes. m6A is composed of 0.1–0.4% adenylate residues, especially at the beginning of 3′-UTR near the translation stop codon. The m6A regulator can be classified into three types, namely the “writer”, “reader”, and “eraser”. Studies have shown that the epigenetic modulation of m6A influences mRNA processing, nuclear export, translation, and splicing. Regulated cell death (RCD) is the autonomous and orderly death of cells under genetic control to maintain the stability of the internal environment. Moreover, distorted RCDs are widely used to influence the course of various diseases and receiving increasing attention from researchers. In the past few years, increasing evidence has indicated that m6A can regulate gene expression and thus influence different RCD processes, which has a central role in the etiology and evolution of MSDs. The RCDs currently confirmed to be associated with m6A are autophagy-dependent cell death, apoptosis, necroptosis, pyroptosis, ferroptosis, immunogenic cell death, NETotic cell death and oxeiptosis. The m6A–RCD axis can regulate the inflammatory response in chondrocytes and the invasive and migratory of MM cells to bone remodeling capacity, thereby influencing the development of MSDs. This review gives a complete overview of the regulatory functions on the m6A–RCD axis across muscle, bone, and cartilage. In addition, we also discuss recent advances in the control of RCD by m6A-targeted factors and explore the clinical application prospects of therapies targeting the m6A–RCD in MSD prevention and treatment. These may provide new ideas and directions for understanding the pathophysiological mechanism of MSDs and the clinical prevention and treatment of these diseases.

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ALKBH5-mediated m6A demethylation of HS3ST3B1-IT1 prevents osteoarthritis progression

Cited by 3 publications

References 47 publications

Recent advances of m6A methylation in skeletal system disease

Recent advances of m6A methylation in skeletal system disease

Transcriptome‐wide RNA m6A methylation profiles in an endemic osteoarthropathy, Kashin‐Beck disease

Novel Insights into the Links between N6-Methyladenosine and Regulated Cell Death in Musculoskeletal Diseases

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