USP34 (Ubiquitin Specific Peptidase 34)

Furthermore, we revealed that DAZAP1 expression is post-transcriptionally regulated by m6A modification through the demethylase ALKBH5, which protects DAZAP1 mRNA from YTHDF2-mediated degradation. Collectively, our findings establish the ALKBH5/DAZAP1/USP34/PIN1/MAPK axis as a key regulatory mechanism in gastric tumorigenesis and chemoresistance, underscoring DAZAP1 as a promising candidate for therapeutic and diagnostic applications in GC.

USP34 is an independent prognostic predictor in AML and may contribute to leukemogenesis via intervening immune processes and promoting proliferation.

Furthermore, paclitaxel-induced apoptosis was verified by altered levels of apoptotic and antiapoptotic proteins including PARP, caspase-3, Bax, Bcl-2, Bcl-XL, and p53. The identification of these DUB genes highlights their potential as biomarkers for predicting drug responsiveness and prognosis during paclitaxel treatment, thereby proposing a new direction for improving the therapeutic efficacy of paclitaxel in NSCLC.

Overexpression of c-Myc reverted the inhibitory effects of si-USP34 on the malignant biological behavior in HCC cells. The USP34 regulates aerobic glycolysis and inhibits the progression of HCC by accelerating c-Myc ubiquitinated degradation.

Mechanistically, lactylation of histones promoted the expression level of USP34 in HepG2/DDP cells. USP34 promotes the progression of HCC by regulating histone lactylation levels and cisplatin resistance in HCC.

This study confirmed that USP34 could upregulate PIN1 expression and SUMOylation, thereby inhibiting ferroptosis by suppressing the cGAS-STING pathway and in turn promoting the progression of cervical cancer.

Finally, the mechanism of FOXC1 regulation by BPTF was found to result from the affected protein stability of FOXC1 through USP34-mediated de-ubiquitylation. In conclusion, the BPTF/FOXC1 axis was identified as a key promotor in glioma development and may be a potential target in the inhibition of glioma development.

Combined inhibition of Pin1 and CDK1 with sulfopin and RO3306 most effectively suppresses orthotopic tumor growth. Our findings provide multiple molecular targets to induce Pin1 degradation and suppress hypersumoylation for cancer treatment.

Although T-ALL and T-LBL both originate from precursor T-cells and are considered different manifestations of the same disease and the outcome of T-LBL is favorable when using T-ALL-based chemotherapy, there are differences in the gene distribution between T-LBL and T-ALL. It seems that the PI3K-Akt signaling pathway and the USP34 gene play important roles in T-LBL, but medicines targeting the USP34 gene or the PI3K-Akt pathway may be invalid.