Emerging roles of JMJD3 in cancer

Farzaneh, Maryam; Kuchaki, Zeinab; Sheykhahmad, Fatima Rashid; Meybodi, Seyed Mohammadmahdi; Abbasi, Yusef; Gholami, Effat; Ghaedrahmati, Farhoodeh; Anbiayee, Omid

doi:10.1007/s12094-021-02773-9

Cited by 9 publications

(7 citation statements)

References 130 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 76 Those changes comprise DNA and histone modifications, known as epigenetic marks. 77 , 78 Such markers are subjoined to particular DNA and histones through various enzymes. 79 Modifications in the epigenomes participate in the instability of chromosomes, supply survival benefits to LSCs, and result in cancer initiation and progression.…”

Section: Dna Repair and Epigenetic Pathways Involved In Lscsmentioning

confidence: 99%

Signaling pathways governing the behaviors of leukemia stem cells

Azizidoost¹,

Nasrolahi²,

Sheykhi-Sabzehpoush³

et al. 2024

Genes & Diseases

Self Cite

View full text Add to dashboard Cite

Section: Dna Repair and Epigenetic Pathways Involved In Lscsmentioning

confidence: 99%

Signaling pathways governing the behaviors of leukemia stem cells

Azizidoost¹,

Nasrolahi²,

Sheykhi-Sabzehpoush³

et al. 2024

Genes & Diseases

Self Cite

View full text Add to dashboard Cite

“…PRMT5 is considered to play a role in cancer progression through the modulation of various oncogenic cellular pathways such as cell proliferation, migration and invasion [ 117 ]. KSHV PF-8 interacts with KSHV long noncoding polyadenylated nuclear RNA (PAN RNA) to recruit host demethylases, namely, ubiquitously transcribed tetratricopeptide repeat on chromosome X (UTX) and Y (UTY) [ 118 , 119 , 120 ]. HPV E7 can also upregulate UTX and UTY causing virally-induced epigenetic reprogramming [ 121 , 122 ].…”

Section: Postulated Oncogenic Roles Of Ebv Lytic Proteinsmentioning

confidence: 99%

Contribution of Epstein–Barr Virus Lytic Proteins to Cancer Hallmarks and Implications from Other Oncoviruses

Dorothea

Xie

Yiu

et al. 2023

Cancers

View full text Add to dashboard Cite

Epstein–Barr virus (EBV) is a prevalent human gamma-herpesvirus that infects the majority of the adult population worldwide and is associated with several lymphoid and epithelial malignancies. EBV displays a biphasic life cycle, namely, latent and lytic replication cycles, expressing a diversity of viral proteins. Among the EBV proteins being expressed during both latent and lytic cycles, the oncogenic roles of EBV lytic proteins are largely uncharacterized. In this review, the established contributions of EBV lytic proteins in tumorigenesis are summarized according to the cancer hallmarks displayed. We further postulate the oncogenic properties of several EBV lytic proteins by comparing the evolutionary conserved oncogenic mechanisms in other herpesviruses and oncoviruses.

show abstract

“…Jumonji domain‐containing protein D3 (JMJD3) belongs to JmjC histone demethylase family, which can regulate gene expression through H3K27me3 demethylation 12 . The involvement of JMJD3 in OA development has been validated by a series of studies.…”

Section: Introductionmentioning

confidence: 99%

“…Jumonji domain-containing protein D3 (JMJD3) belongs to JmjC histone demethylase family, which can regulate gene expression through H3K27me3 demethylation. 12 The involvement of JMJD3 in OA development has been validated by a series of studies. For example, knockdown of JMJD3 ameliorated aberrant force-induced OA via epigenetic regulation of nuclear receptor subfamily 4 group A member 1 through H3K27me3 demethylation.…”

mentioning

confidence: 96%

SKP2‐mediated ubiquitination and degradation of KLF11 promotes osteoarthritis via modulation of JMJD3/NOTCH1 pathway

Huang,

Pan,

2024

The FASEB Journal

View full text Add to dashboard Cite

Osteoarthritis (OA) is the main cause of cartilage damage and disability. This study explored the biological function of S‐phase kinase‐associated protein 2 (SKP2) and Kruppel‐like factor 11 (KLF11) in OA progression and its underlying mechanisms. C28/I2 chondrocytes were stimulated with IL‐1β to mimic OA in vitro. We found that SKP2, Jumonji domain‐containing protein D3 (JMJD3), and Notch receptor 1 (NOTCH1) were upregulated, while KLF11 was downregulated in IL‐1β‐stimulated chondrocytes. SKP2/JMJD3 silencing or KLF11 overexpression repressed apoptosis and extracellular matrix (ECM) degradation in chondrocytes. Mechanistically, SKP2 triggered the ubiquitination and degradation of KLF11 to transcriptionally activate JMJD3, which resulted in activation of NOTCH1 through inhibiting H3K27me3. What's more, the in vivo study found that KLF11 overexpression delayed OA development in rats via restraining apoptosis and maintaining the balance of ECM metabolism. Taken together, ubiquitination and degradation of KLF11 regulated by SKP2 contributed to OA progression by activation of JMJD3/NOTCH1 pathway. Our findings provide promising therapeutic targets for OA.

show abstract

Emerging roles of JMJD3 in cancer

Cited by 9 publications

References 130 publications

Signaling pathways governing the behaviors of leukemia stem cells

Signaling pathways governing the behaviors of leukemia stem cells

Contribution of Epstein–Barr Virus Lytic Proteins to Cancer Hallmarks and Implications from Other Oncoviruses

SKP2‐mediated ubiquitination and degradation of KLF11 promotes osteoarthritis via modulation of JMJD3/NOTCH1 pathway

Contact Info

Product

Resources

About