WSB1 (WD Repeat And SOCS Box Containing 1)

While the precise mode of intercellular transfer remains to be elucidated, these findings suggest the involvement of extracellular vehicles or other secretory pathways. This strategy may offer a novel therapeutic avenue for targeting KRAS-driven tumors, particularly pancreatic adenocarcinoma.

Importantly, disruption of the WSB1/OTUD4/ISOC2 axis upregulated P16INK4a expression, and co-silencing of P16INK4a partially restored tumorigenic properties. Our findings unveil a novel WSB1/OTUD4/ISOC2 signaling network that drives prostate cancer progression by modulating ubiquitin signaling and repressing P16INK4a, positioning WSB1 as a promising therapeutic target.

Taken together, our results identify the DIO2 degradation by WSB1 and subsequent impairment of T3/TRβ1 signaling as mechanisms leading to LM in CRC. These findings can inform therapeutic interventions for this event.

Okanin does not change the body weight of the animals; in comparison, 5-fluorouracil reduces the body weight, despite being less effective...Okanin is a promising investigational drug. PRDX5 and GPX4 are candidate targets for cancer chemotherapy, at least for colorectal cancer.

This study successfully established and validated a novel 13-gene signature, a valuable marker for predicting cervical cancer patient survival.

Our recent work demonstrates that WSB1 and WSB2 (WSB1/2), two additional SOCS-box proteins with structurally similar WD40 repeat domains, function as substrate-recognizing subunits of ECSWSB1/2 to specifically mediate the ubiquitination and degradation of chromatin-associated RelA methylated at Lys314/315. In this review, we summarize the discovery and functional importance of ECSSOCS1 and ECSWSB1/2 in terminating NF-κB activity, highlight the distinct molecular mechanisms by which they ubiquitinate chromatin-associated RelA in a modification- and gene-specific manner, and discuss their potential as therapeutic targets for inflammatory diseases and cancer.

WSB1 mRNA stability was measured by Actinomycin D. Elevated expressions of HNRNPL and WSB1 were found in both ccRCC tissues and cells...Rescue assay identified the promotive effect of HNRNPL on lipid droplets and cell proliferation of ccRCC cells can be abolished in response to WSB1 knockdown. Collected evidence summarized that HNRNPL can increase the stability of WSB1 mRNA to promote lipid droplet and proliferation ability in ccRCC cells.

circWSB1 diminishes the inhibitory impact of miR-182-5p on WSB1 and increases WSB1 expression, thereafter promoting ccRCC development. Our findings provide a promising predictive biomarker and therapeutic target for ccRCC.

Our study is the first to show a link between WSB1 expression and other genes involved in PC progression, suggesting a novel role for WSB1 in PC progression. This network between WSB1 and EZH2 through WNT/β-catenin may have an important role in PC progression, as suggested by the association between high WSB1 expression and unfavorable prognosis in our analysis.

The histological analyses show that PIN1 and CDK1 are highly expressed in TNBC samples, which negatively correlate with the expression of pVHL. Taken together, our findings reveal the previous unrecognized tumor-promoting function of CDK1/PIN1 axis through destabilizing pVHL and provide the preclinical evidence that targeting CDK1/PIN1 is an appealing strategy in the treatment of multiple cancers with wild-type VHL.

Moreover, overexpressing WSB1 in the Bel-7402 xenograft model could further strengthen the tumor-driven effect of c-Myc overexpression. Thus, our findings revealed a novel mechanism involved in tumorigenesis in which the WSB1/c-Myc feedforward circuit played an essential role, highlighting a potential c-Myc intervention strategy in cancer treatment.