Genome-wide DNA methylation profiling of articular cartilage reveals significant epigenetic alterations in Kashin-Beck disease and osteoarthritis

Wang, W.; Yu, Yan; Hao, Jingcan; Wen, Yan; Han, Jing; Hou, Weikun; Liu, R.; Zhao, Bo; He, Awen; Li, P.; Fan, Qunping; Wu, Chunyu; Wang, S.; Wang, X.; Ning, Yujie; Guo, Xiong; Zhang, Feng

doi:10.1016/j.joca.2017.08.002

Cited by 27 publications

(17 citation statements)

References 29 publications

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“…In line with chondrosarcomas, accumulating evidence also shows epigenetic dysregulation in OA [ 180 , 181 ]. However, IDH mutations have not been detected in AC so far, but inflammatory cytokines suppressed IDH and TET activity in human primary chondrocytes in vitro [ 182 ], a mechanism which might also apply in chondrosarcomas without IDH mutation.…”

Section: Chondrosarcoma Treatmentmentioning

confidence: 97%

Chondrosarcoma: A Rare Misfortune in Aging Human Cartilage? The Role of Stem and Progenitor Cells in Proliferation, Malignant Degeneration and Therapeutic Resistance

Boehme

Schleicher

Traub

et al. 2018

IJMS

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Unlike other malignant bone tumors including osteosarcomas and Ewing sarcomas with a peak incidence in adolescents and young adults, conventional and dedifferentiated chondrosarcomas mainly affect people in the 4th to 7th decade of life. To date, the cell type of chondrosarcoma origin is not clearly defined. However, it seems that mesenchymal stem and progenitor cells (MSPC) in the bone marrow facing a pro-proliferative as well as predominantly chondrogenic differentiation milieu, as is implicated in early stage osteoarthritis (OA) at that age, are the source of chondrosarcoma genesis. But how can MSPC become malignant? Indeed, only one person in 1,000,000 will develop a chondrosarcoma, whereas the incidence of OA is a thousandfold higher. This means a rare coincidence of factors allowing escape from senescence and apoptosis together with induction of angiogenesis and migration is needed to generate a chondrosarcoma. At early stages, chondrosarcomas are still assumed to be an intermediate type of tumor which rarely metastasizes. Unfortunately, advanced stages show a pronounced resistance both against chemo- and radiation-therapy and frequently metastasize. In this review, we elucidate signaling pathways involved in the genesis and therapeutic resistance of chondrosarcomas with a focus on MSPC compared to signaling in articular cartilage (AC).

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Section: Chondrosarcoma Treatmentmentioning

confidence: 97%

Chondrosarcoma: A Rare Misfortune in Aging Human Cartilage? The Role of Stem and Progenitor Cells in Proliferation, Malignant Degeneration and Therapeutic Resistance

Boehme

Schleicher

Traub

et al. 2018

IJMS

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“…They identified 45 genes with significant DNA methylation differences, including three genes which were hypomethylated in both OA and RA patients 14 . The second, by Wang and colleagues, was a small study which included five OA, five normal (neck of femur fracture), and five Kashin-Beck disease (KBD), an endemic osteochondropathy associated with accelerated OA in Siberia, Korea, and China 15 . They identified several differentially methylated positions (DMPs) by Illumina 450 k array associated with both KBD and OA, including 367 which overlapped (were associated with both OA and KBD), corresponding to 182 genes, all with matching methylation directions in both OA and KBD (i.e., hypermethylated or hypomethylated in both compared to control).…”

Section: Epigenetics: Dna Methylationmentioning

confidence: 99%

Osteoarthritis year in review 2018: genetics and epigenetics

Jeffries

2019

Osteoarthritis and Cartilage

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Objective: This review was designed to identify highlights of the osteoarthritis (OA) genetics and epigenetics literature published between April 2017 and January 2018. Design: A Pubmed literature search was conducted using the keywords 'osteoarthritis' and each of the following: 'genomic', 'genetic', 'epigenomic', 'epigenetic', 'histone', 'noncoding RNA', 'miRNA', 'lncRNA', 'DNA methylation', 'DNA hydroxymethylation', 'DNMT', and 'TET'. The dates of publication were restricted to 4/1/2017e1/15/2018. Results were compared to the same search terms limited to 4/1/2016e1/15/2017. Results: Virtually all search term combinations demonstrated a decrease in papers published this year compared to last, with epigenetic and miRNA/lncRNA research being stable. Despite this, numerous advances were made this year, including the second large genome-wide association study (GWAS) study of hand OA, a new twin study of hip and knee OA concordance, an extensive study of GDF5 evolution, analyses of the contribution of Dnmt3a to OA, a description of DNA methylation in a nonhuman primate model of OA, and an integrated, multi-omics analysis of DNA methylation, mRNA, and protein expression in human OA samples, among others. A variety of micro-and a few circular-RNA studies were also published, highlighting the importance of noncoding RNA in both the pathogenesis and potential treatment of OA. Conclusion: Although publications have decreased slightly in the last year, genetics and epigenetics continue to be a topic of substantial research in OA, and considerable progress continues to be made in the field.

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“…Some studies suggested that some genes might contribute to the development of KBD, such as GPX1 , [10] GPX4 , [11] SELS , [9] SEPP , [12] ADAM12 , [13] Col2A1 , [14] Bcl-2 , Bax , and Fas . [15] But these studies only provided a limited explanation for the KBD occurrence and insufficiently revealed their roles and functions in the development of KBD. In the whole genome-wide, these genes do not play independent roles; instead, these genes form biological function and pathway networks through their intricate interactions, which can give us a more complete picture of their genetic function contributing to the development of KBD.…”

Section: Introductionmentioning

confidence: 99%

Pathway-based network analyses and candidate genes associated with Kashin-Beck disease

et al. 2019

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Genome-wide DNA methylation profiling of articular cartilage reveals significant epigenetic alterations in Kashin-Beck disease and osteoarthritis

Abstract: Our data implicate epigenetic dysregulation of a host of genes in KBD and OA. Furthermore, we observed common causal epigenetic changes shared by KBD and OA.

Cited by 27 publications

References 29 publications

Chondrosarcoma: A Rare Misfortune in Aging Human Cartilage? The Role of Stem and Progenitor Cells in Proliferation, Malignant Degeneration and Therapeutic Resistance

Chondrosarcoma: A Rare Misfortune in Aging Human Cartilage? The Role of Stem and Progenitor Cells in Proliferation, Malignant Degeneration and Therapeutic Resistance

Osteoarthritis year in review 2018: genetics and epigenetics

Pathway-based network analyses and candidate genes associated with Kashin-Beck disease

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