YOD1 (YOD1 Deubiquitinase)

RUNX2 inhibition reduces PAX3::FOXO1 expression and signaling, which impairs fusion-positive rhabdomyosarcoma oncogenic phenotypes. In vivo treatment with CADD522 decreased tumor growth and increased survival, indicating that RUNX2 is a promising therapeutic target.

Furthermore, overexpression of YOD1 reversed the tumor-suppressive effects observed after SOX21-AS1 knockdown. In conclusion, SOX21-AS1 promotes PC cell malignancy through the miR-9-3p/YOD1 axis and subsequent activation of TGF-β/Smad signaling.

In ISO-treated cardiomyocytes, pretreatment with PKM2 activator TEPP-46 (20 μM) reversed YOD1 overexpression-induced hypertrophy and OXPHOS inhibition. This study reveals a new YOD1-PKM2 axis in cardiomyocytes and identifies YOD1 as a potential target for the treatment of ISO-induced cardiac remodeling and heart failure.

Patients with MYOD1 mutations have an extremely poor prognosis, which is independent of clinical staging and grading. MYOD1 mutation detection in rhabdomyosarcoma has significant value for auxiliary diagnosis and prognostic assessment.

A subset of five cases were stained for PAX7, and a single case of malignant OFMT showed weak expression. To our knowledge, this is the first formal study of rhabdomyoblastic marker expression in OFMT.

Importantly, reduced YOD1 and ZNF24 levels were strongly associated with poor clinical outcomes in ccRCC patients. Our results reveal the mechanism by which YOD1 regulates VEGFA transcription and suppresses tumorigenesis by deubiquitinating ZNF24, providing a therapeutic target in ccRCC.

The major drawback of considering YOD1 as a biomarker or therapeutic target is that its tumour-regulatory role is mainly based on the findings from single-center studies with relatively small sample sizes. Hence, future large-scale and in-depth clinical trials should be conducted to further verify the translational values of YOD1 as a biomarker or therapeutic target.

The BIK knockdown rescued the effects of MyoD1 overexpression on GC cells. In conclusion, MyoD1 inhibited cell proliferation via 158 genes and 47 lncRNAs downstream directly or indirectly that participated in multiple signaling pathways in GC, and among these, MyoD1 promotes BIK transcription by binding to its promoter, then promotes BIK-Bcl2-caspase 3 axis and regulates GC cell apoptosis.

Oral administration of β-catenin inhibitor MSAB (20 mg/kg, every other day for four weeks) eliminated the protective effect of YOD1 deletion on vascular endothelial injury. In conclusion, we demonstrate a new YOD1-β-catenin axis in regulating Ang II-induced vascular endothelial injury and reveal YOD1 as a deubiquitinating enzyme for β-catenin, suggesting that targeting YOD1 holds promise as a potential therapeutic strategy for treating β-catenin-mediated vascular diseases.

Its prognosis is better than other subtypes of rhabdomyosarcoma and those in adolescents and adults with the same subtype. Analysis and summary of its clinicopathological features can help differentiate it from other soft tissue tumors in infants and children and provide the information for appropriate treatments.

Their genetic hallmark is the presence of EWSR1/FUS-TFCP2 fusions. Familiarity with its clinicopathological characteristics is helpful in avoiding misdiagnoses.

These results indicated that TRIM54 played a critical role in reducing the effects of tendon injury. Consequently, these results shed light on potential therapeutic alternatives for treating tendinopathy.