USP44 (Ubiquitin Specific Peptidase 44)

Our study identifies and validates a novel four-gene ubiquitination-related signature as a promising and independent prognostic biomarker in THCA. Beyond outcome prediction, this signature demonstrates significant translational potential by accurately predicting immunotherapy responses, thereby facilitating the development of more personalized and effective treatment strategies for patients with THCA.

USP44-SENP2 axis is a pivotal factor in the progression of ESCC, and provides potential therapeutic targets for ESCC patients.

Further studies are needed for clinical application of liquid biopsy using methylation analysis for ctDNA according to individual characteristics for breast cancer.

In addition, ITGB4 affects the expression of P-gp and the activity of antioxidant enzymes through the MAPK/NF-κB pathway, thereby promoting cisplatin efflux and chemoresistance. Our research uncovers a novel mechanism behind cisplatin resistance and indicates that USP44 could be a promising therapeutic target for overcoming cisplatin resistance in gastric cancer patients.

Notably, treatment with GSK126, a specific EZH2 inhibitor, reversed the chemoresistance induced by USP44 overexpression. USP44/EZH2 signaling pathway is one of the key to causing the drug resistance of TNBC, warranting further clinical investigation.

This discriminatory biomarker panel algorithm exemplifies a practical nonendoscopic strategy to diagnose BE, HGD, and EAC using a minimally-invasive sponge-capsule device coupled with DNA methylation markers.

At the same time, HEXIM1 knockdown reversed the antitumor effects of USP44. These findings demonstrated that USP44 acted as a critical tumor suppressor in OSCC by inhibiting cell proliferation and metastasis through the stabilization of HEXIM1 protein, suggesting that USP44-HEXIM1 axis is a promising target for OSCC therapy.

Overexpression of WDR5 reversed the growth inhibition of CSRP2 overexpression on prostate cancer cells. Altogether, our data indicate that CSRP2 suppresses prostate cancer cell proliferation via a CSRP2/WDR5/USP44 dependent pathway to control prostate cancer progression, suggesting a potential mechanism for prostate cancer treatment.

In addition, the rescue of p21 partially alleviated cell cycle advancement and cell proliferation induced by the depletion of USP44. Our findings, taken together, indicate that USP44 is frequently repressed in thyroid cancer due to promoter hypermethylation and functions as a tumor suppressor by stabilizing p21 via deubiquitination.

Our findings demonstrate that the USP44-STUB1-LRPPRC axis plays a pivotal role in neuroblastoma chemoresistance and provides potential targets for neuroblastoma therapy and prognostication.

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.

GC cells were treated with MG132 and the ubiquitination level of CTCFL was examined using ubiquitination assay...Overexpression of USP44 and CTCFL attenuated the inhibitory effects of miR-98-5p overexpression on GC cell progression. miR-98-5p overexpression limited USP44-mediated CTCFL deubiquitination, and suppressed CTCFL expression, mitigating GC cell proliferation, migration, and invasion.