CUL1 (Cullin 1)

In MDA-MB-231 xenografts, compound 30 significantly inhibited tumor growth in a dose-dependent manner without observable toxicity. These findings highlight compound 30 as a promising therapeutic candidate for TNBC treatment through CSN5 inhibition, which simultaneously induces PD-L1 degradation and direct antitumor activity.

DCUN1D5 contributes to the growth and motility of CRC in vitro and in vivo.

Inhibiting ERK5 reversed the beneficial effects of MLN4924 on inflammation, BBB disruption, and neurobehavioral deficits. Collectively, inhibition of the NEDD8 pathway by MLN4924 attenuates inflammation, BBB disruption, and neurological deficits via the p-ERK5-KLF2-ICAM-1 axis, highlighting NEDD8 pathway as a potential therapeutic target for ICH.

Together, our findings demonstrate that CUL1-IPA, an IPA-derived long noncoding RNA (lncRNA), forms an RNA-protein complex in the nucleolus to support nucleolar structure and function. This study provides an insight into the biological function of a lncRNA originating from a protein-coding gene and highlights the broader significance of IPA-derived noncoding RNAs as regulatory molecules.

Finally, we highlight the clinical potential of FBXO31 in human malignancies, discussing its implications as both a biomarker and a therapeutic target. In conclusion, understanding the nuanced biology of FBXO31 is crucial for unravelling its role in tumorigenesis and advancing future therapeutic strategies.

In conclusion, CUL1 was significantly overexpressed in CRC, correlating with disease progression, treatment response, and poor prognosis. Overall, these findings suggest CUL1 as a prognostic marker and a potential therapeutic target for patients with CRC.

In a human xenograft model, depletion of FBXO11 cooperated with AML1-ETO and mutant KRASG12D to generate serially transplantable AML. Our findings suggest that reduced FBXO11 cooperates to initiate AML by priming HSPC for myeloid-biased self-renewal through attenuation of LONP1-mediated regulation of mitochondrial respiration.

In conclusion, our comprehensive analysis revealed that FBXO2 plays a critical tumor-suppression role in BRCA, with its down-regulation contributing to poor prognosis. Furthermore, FBXO2 was implicated in immune regulation and tumor microenvironment remodeling. Our findings provided novel insights into the pathogenesis of BRCA.

Current strategies under investigation include small-molecule inhibitors (SMIs) and RNA interference (RNAi). This review highlights recent advances in understanding the molecular mechanisms of F-box proteins in breast cancer and explores their potential in targeted therapy.

The results showed that the relative gene expression levels of MKN45 and AGS cell lines were higher than those in the GES-1 cell line in the control., and the results were aligned with the in silico findings. CDK1, CDK2, NOXO1, CUL1, MAPK1, and CCNB1 play pivotal roles in GC carcinogenesis and hold promise as early diagnostic biomarkers and therapeutic targets for GC.

Stabilization of MCL1 and HAX1 by RPS4X led to increased resistance of HeLa cells to doxorubicin-induced apoptosis. These findings suggest that RPS4X contributes to the regulation of protein homeostasis and apoptotic pathways by modulating SCF complex activity, providing new insights into the extraribosomal roles of ribosomal proteins.

Collectively, our findings identify the FBXO22 SCF complex as a key negative regulator of TRIM48-driven ASK1-activation and cell death under oxidative stress. The dysregulation of this axis may underlie human-specific pathologies, such as tumorigenesis and oxidative stress-associated disorders, highlighting its potential as a target for novel therapeutic interventions.