OTUD6B (OTU Deubiquitinase 6B)

[This retracts the article DOI: 10.1155/2020/3035624.].

Bioinformatics analysis demonstrates that these DUBs except USP47 are upregulated and overall survival analysis indicates that lower expression of these DUBs, except USP37 and USP49, is correlated with improved overall survival in lung cancer patients. These findings strongly suggest that DUBs may play a crucial role in overcoming cisplatin resistance and improving the treatment efficacy for lung cancer.

Moreover, we found that pharmaceutical Kv11.1 opening produced a rapid proteasomal degradation of c-Myc and that this could be antagonized by the OTUD6B deubiquitinase. We concluded that use of Kv11.1 agonists should be considered as anticancer pharmacological strategy against lung adenocarcinomas.

More in vivo and in vitro studies on OTUDs may contribute to the development of inhibitors or agonists targeting OTUDs. Of course, when conducting these studies, researchers also need to pay attention to the impact of OTUDs on the host's antiviral immune response.

In conclusion, OTUD6B-AS1 serves as a biomarker in BC, driving immune evasion and ferroptosis resistance. Targeting OTUD6B-AS1 may enhance immunotherapy efficacy and overcome chemoresistance, offering novel therapeutic avenues.

Ectopically expressed DDX5 facilitated transcription factor STAT3 activation by resolving the RNA G-quadruplex structure of STAT3, resulting in a higher level of CXCL11 transcription and an increase in tumor-infiltrating CD8+ T cells. All-trans retinoic acid inhibited CRLM by upregulating OTUD6B.

Additionally, we assess the clinical relevance of OTUD6B-AS1 expression levels, evaluating its potential as a biomarker for cancer prognosis and diagnosis, as well as a target for therapeutic intervention. By consolidating existing knowledge, this work aims to highlight the clinical implications of OTUD6B-AS1 and encourage further research in oncology, ultimately contributing to the advancement of targeted cancer therapies.

Indeed CRISPR-Cas9 editing results in only OTUD6B-/+ TNBC cells which fail to divide and die. As a deubiquitinase that supports KIFC1 expression, allowing pseudo-bipolar cell division and survival of cancer cells with centrosome amplification, OTUD6B has potential as a novel target for cancer-specific therapies.

Specifically, we examined the therapeutic effects of siOTUD6B and doxorubicin (DOX) co-delivery using synthesized tetrahedral DNA nanoparticles (Tds) on tumor growth and progression...Mechanistically, OTUD6B regulates TNBC progression by stabilizing murine double minute 2 (MDM2) and degrading forkhead box O3a (FOXO3a). Conclusively, this study demonstrates the potential applicability of DNA nanoparticles loaded with DOX and siOTUD6B for TNBC treatment.

Our study demonstrates that OTUD6B knockdown participates in the ubiquitination of PTK2 and phosphorylation of STAT3 to alleviate the process of CCA. These results suggest that OTUD6B may be a potential new strategy for CCA treatment.

Collectively, our findings indicate the involvement of circPTPN12 in modulating PDLIM2 function, influencing HCC progression. The identified ESRP1/circPTPN12/PDLIM2/NF-κB axis shows promise as a novel therapeutic target in the context of HCC.

Our results suggest that OTUD6B is a promising clinical target for LUAD treatment and that targeting OTUD6B may constitute an effective anti-LUAD strategy.