FBXO31 (F-Box Protein 31)

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.

The regulatory roles of Thr-37 and Ser-523 in FBXO31 stability are associated with variations in phosphorylation levels and degradation pathways. These results demonstrate that phosphorylation regulates FBXO31 turnover, and phosphorylation at Thr-37 or Ser-523 may help identify upstream kinases and enhance the understanding of the physiological role of FBXO31.

In vivo experiment further showed that CD147 (+) cells promoted tumor growth and metastasis, while after transfection with FBXO31, tumor proliferation and metastatic abilities were inhibited. Overall, FBXO31 inhibits the migration, invasion, and stemness characteristics of CD147 (+) melanoma stem cells.

Downregulation of O-GlcNAcylation impedes EC tumor formation in mouse models. Collectively, our study highlights O-GlcNAcylation as a useful stratification marker and a therapeutic vulnerability for the advanced, poorly differentiated EC cases.

Modest impact on steady-state SKP1 modification levels suggests that effects are mediated during a lag phase in hydroxylation of nascent SKP1. The dependence of FBP abundance on O2-dependent SKP1 modification likely contributes to the reduced virulence of PHYaΔ parasites owing to impaired ability to sense O2 as an environmental signal.

Furthermore, KLF9 promoted FBXO31 transcription. Overall, the present study suggested that the KLF9-mediated regulation of FBXO31 could inhibit the progression of EC and enhance the sensitivity of EC cells to DDP.

The results showed that METTL3 enhanced FBXO31 mRNA translation in YTHDF1-dependent manner. Taken together, we suggest that METTL3-FBXO31-SIRT2 axis was involved in PC tumorigenesis, which could identify new targets for PC treatment.

miR-3677-3p down-regulation or FBXO31 overexpression promoted the ubiquitylation of FOXM1. In a word, miR-3677-3p bound to FBXO31 and inhibited FBXO31 expression, thus curtailing the ubiquitylation degradation of FOXM1, contributing to HCC development and sorafenib resistance.

ZNF529-AS1 could be a new prognostic marker for HCC. FBXO31 may be the downstream target of ZNF529-AS1 in HCC.