FBXO11 (F-Box Protein 11)

These findings identify LAMP5 as a multifunctional oncoprotein with both prognostic and therapeutic relevance in bladder cancer. This study provides insights into the molecular mechanisms by which LAMP5 promotes bladder cancer progression and offers potential targets for therapeutic intervention and clinical management.

Finally, we discovered rare mutations in FBXO11, which mapped to a previously unstudied functional intrinsically disordered region (IDR) in the N-terminus responsible for binding NPM1. These data support a model in which FBXO11 rewires RNA binding and ribosomal subnetworks through ubiquitylation of NPM1, ultimately restricting MDS progression.

This aberrant PRMT9 expression is governed by IGF2BP1-mediated m6A modification. These findings suggest that therapeutic targeting of PRMT9 or the RAS/MAPK signaling axis may represent a promising strategy for LUAD treatment.

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.

FBXW11 promotes the progression of AP by enhancing IRF1 transcription through the ubiquitination-mediated degradation of HIC1. Inhibition of FBXW11 or HIC1 effectively reduces the production of inflammatory cytokines and decreases cell apoptosis, thereby alleviating the symptoms of AP.

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.

This study identifies a previously unrecognized master regulator CCNC that functions as a suppressor of CD155-mediated cancer immune evasion. The findings of this study suggest that tumors with low CCNC expression may be resistant to monotherapy and highlight a combination immunotherapy (TIGIT/PD-1 co-blockade) as a promising anti-cancer therapeutic strategy to overcome immune evasion in CCNC-deficient tumors.

This study elucidates specific features associated with the p53 regulatory pathway, particularly SMYD2, and its relationship with the onset and progression of CESC. Furthermore, SMYD2 may serve as a prognostic biomarker for individuals diagnosed with CESC, offering new insights for the development of clinical treatment strategies.

The ancillary testing of SMARCB1 (INI-1) should be considered in a subset of patients whose tumor demonstrates bizarre cytomorphology, especially in poorly differentiated or markedly pleomorphic tumors. The cytological recognition is critical for appropriate management.

hnRNPA3 stabilizes GLI2 by disrupting its interaction with FBXW11, thereby enhancing Hh pathway activity and contributing to HCC progression. These findings position hnRNPA3 as a potential prognostic biomarker and therapeutic target for HCC, warranting further investigation.

Collectively, our findings demonstrate that Rut ameliorates AP by upregulating EZH2, thereby enhancing H3 methylation and suppressing FBXW11 expression.

FBXW11 acts as a tumor suppressor in HCC by mediating YB1 ubiquitination and degradation, thereby inhibiting the Akt/mTOR pathway. The FBXW11-YB1 axis represents a novel regulatory mechanism in hepatocarcinogenesis, highlighting FBXW11 as a potential prognostic biomarker and therapeutic target for HCC.