CCNF (Cyclin F)

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.

It may serve as a potential biomarker for diagnosis, patient stratification, and guiding personalized therapy. Further research could enhance SOC management.

Taken together, our findings establish FBXO5 as a critical mediator of CRPC progression and bone metastatic potential, underscoring its importance as a promising therapeutic target for this aggressive disease.

We utilized single-particle cryoelectron microscopy to elucidate the structure of a Cyclin F-Skp1 complex bound to an E2F1 peptide. The structure and biochemical analysis reveal important differences in the substrate-binding site of Cyclin F compared to Cyclin A. Our findings expand on the canonical cyclin-binding motif (Cy or RxL) and highlight the importance of electrostatics at the E2F1 binding interface, which varies between Cyclin F and Cyclin A. These results advance our understanding of E2F1 regulation and may inform strategies for selectively targeting Cyclin F in cancer or neurodegeneration.

To assess the role of FBXO11 in OC cells, we established stable human OC cell lines with tetracycline-inducible (Tet-on) expression of FBXO11 CDS or shRNA...In summary, FBXO11 functions as a tumor suppressor in OC through ubiquitin-proteasomal degradation of KIF2C; and the low expression level of FBXO11 in OC may be attributed to its transcriptional inhibition by transcription factor ZNF217. These findings provided new insights into understanding the molecular mechanism of OC progression.

NRXN3 plays a crucial role in maintaining chemotherapy-induced pyroptosis in ICC. Targeting the NRXN3/RSK1/FBXO1/caspase-3 axis emerges as a promising strategy for ICC treatment, with the potential to improve chemosensitivity and survival.

CDH1 promotes the entry of colorectal cancer cells into quiescence and enhances stemness by dampening SIRT5 ubiquitination.

Further correlation analysis indicated that CDC20 was positively correlated with the expression of the key genes mTOR, S6K1, and 4E-BP1 and the autophagy-related gene ULK1 in the mTORC1 signaling pathway. These key E3 ubiquitin ligases serve as potential molecular biomarkers for predicting the prognosis, immune response, and drug sensitivity of LUAD patients.

The present results unequivocally demonstrate the availability of four genotoxic marker genes ((Bax, Btg2, Ccng1, and Cdkn1a) and PCA in discriminating GTHCs from NGTHCs and NGTNHCs in Open TG-GATEs. These findings strongly support our recommendation that future rat liver in vivo toxicogenomics tests prioritize these four genotoxic marker genes, as they have proven to be highly effective in discriminating between different types of hepatocarcinogens.

Our analysis identified AIMS subtype and HER2 IHC classification switches from primary BC to BM in matched pairs that could be relevant for prognosis and treatment decisions. In addition, our preliminary differential gene expression analyses showed clear differences in various cellular processes between BC and BM tissues. Whether these differences reflect a selection process or rather an adaptation mechanism to a new environment remains to be investigated.

The mitosis-related gene model serves as a valuable indicator for predicting survival outcomes in colon cancer patients.

The 15 hub genes were expressed across various cell types, and interactions between different cell types were observed. Our study reveals the intricate communication between tumor microenvironment components and tumor metastasis in osteosarcoma.