RNF20 (Ring Finger Protein 20)

There, it recognizes the degron motifs of RIG-I and MDA5 through its coiled-coil domain and catalyzes their K27-linked ubiquitination and degradation, thereby preventing excessive antiviral signaling. These findings shed light on the significant and dual regulatory roles of RNF20 in maintaining innate immune homeostasis.

In addition, two germinal likely pathogenic variants have been identified in the Neurofibromin 1 (NF1) and succinate dehydrogenase complex flavoprotein subunit A (SDHA) genes. Our data suggest a possible additional role of the WAC variant in early tumor development, highlighting the importance of oncogenetic testing in patients with rare neurodevelopmental syndromes and brain tumors.

MEL suppresses the metastasis of NSCLC by targeting USP10 and promoting RNF20-mediated ubiquitination and degradation ofPSMA7.

These include the knockout of SLC29A2, SGMS1, CRLS1, and the RNF20-RNF40 complex, alongside upregulation of CERK and PIKFYVE. The proposed integrative strategy offers novel therapeutic avenues that address both tumor progression and cancer-associated cachexia, with improved specificity and reduced off-target effects, thereby contributing to translational oncology.

RNF20-silenced A549 cells exhibited heightened sensitivity to both the Cisplatin and PARP inhibitor Olaparib. These findings provide an important foundation for further understanding the molecular mechanisms of lung adenocarcinoma and developing new treatment strategies.

Mechanistically, Rnf20 knockdown in adipocytes reduced H3K4me3 occupancy at the Slc2a4 gene locus, inhibiting GLUT4 expression and inducing adipose-specific insulin resistance. These findings establish a critical role for adipocyte RNF20 in the insulin signalling regulation via the H2Bub-H3K4me3-Slc2a4 axis, highlighting its importance in systemic glucose metabolism.

Mechanistically, Rnf20 haploinsufficiency results in inadequate tumor suppression via the Rnf20-H2Bub1-p53 axis and induces DNA damage, cell growth, epithelial-mesenchymal transition (EMT), and metabolic rewiring through HIF1α-mediated RNA polymerase II promoter-proximal pause release, which is independent of H2Bub1. Importantly, decreased RNF20 levels correlate with increased expression of HIF1α and its target genes, suggesting HIF1α inhibition as a promising therapeutic approach for lung cancer patients with reduced RNF20 activity.

The stability of circRNF20 was tested after treatment with actinomycin D. A nude mouse xenograft tumor model was established to validate the effect of IGF2BP2 in vivo...The overexpression of circRNF20 or CDCA4 abolished the inhibitory effect of IGF2BP2 silencing on BC cell proliferation. In conclusion, the binding of IGF2BP2 to circRNF20 prevents its degradation, thus facilitating BC cell proliferation via the HuR/CDCA4 axis.

We conclude that USP44 is a novel epigenetic regulator that promotes aggressive features and may be a novel target in neuroblastoma. Implications: This study identifies a new genetic marker of aggressive neuroblastoma and identifies the mechanisms by which its overactivity contributes to pathophysiology in this disease.

Our study demonstrated that the serum RNF20 expression level was down-regulated in liver cancer, and promoted postoperative survival rate. RNF20 can reduce cancer progression of liver cancer by NLRP3 signal pathway, suggesting that it may prove to be a potential therapeutic target for postoperative survival rate of liver cancer.

Mutational experiments suggest that the two RING domains bind in two orientations and that ubiquitination occurs when Bre1A binds to the acidic patch. Our results provide insights into the H2BK120-specific ubiquitination by the Bre1 proteins and suggest that H2B monoubiquitination can be regulated by nuclesomal DNA flexibility.