FBXO5 (F-Box Protein 5)

CircUSP36 promotes FBXO5 expression by targeting and inhibiting miR-520d-5p, thereby driving cervical cancer cell proliferation, invasion, and migration. The online version contains supplementary material available at 10.1007/s10616-025-00852-1.

FBXO5 promoted TP53 degradation to regulate osteogenic differentiation in hSCAPs, which contributed to AP progression. Targeting FBXO5 may provide a potential therapeutic strategy for AP.

Overexpression of FBXO5 attenuated the antitumor effects of TPs, indicating that TPs partially inhibit HCC progression by suppressing FBXO5. FBXO5 functions as an oncogene in HCC, and TPs may serve as potential therapeutic agents for inhibiting HCC progression by targeting FBXO5.

This compound was found to synergistically improve TMZ sensitivity both in vitro and in vivo. Our results highlight a critical proteasome-cytomechanics pathway in GBM chemoresistance and suggest that targeting FBXO5 could be an effective therapeutic strategy for treating patients with GBM.

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.

Additionally, this study uncovers a small molecule FBXO5 stabilizer that disrupts the β-TrCP1-FBXO5 interaction, thereby markedly enhancing NSP7 degradation and effectively mitigating SARS-CoV-2 infection. Taken together, the findings reveal a novel mechanism for NSP7 regulation and suggest that small-molecule activators of the E3 ubiquitin ligase FBXO5 represent a promising new class of host-directed antiviral therapies.

The bromodomain inhibitor CPI203 induced relatively consistent effects on gene expression and growth across a variety of glioblastoma lines, specifically down-regulating genes associated with DNA replication. We propose that clinically effective BET inhibitors have the potential to induce consistent beneficial effects across a spectrum of glioblastomas.

This indicates that hTERT variants induce TRF2-mediated telomere compaction that is independent of telomere length, and it plays a dominant role in regulating the DNA damage signaling that induces senescence and blocks replication of human fibroblasts. These observations support the idea that very short telomeres often seen in cancer cells may fail to induce senescence due to selective stabilization of components of the shelterin complex, increasing telomere density, rather than maintaining telomere length via the reverse transcriptase activity of hTERT.

This shows that a cell can co-opt the cell cycle genetic program and regulate only certain elements to qualitatively and quantitatively divert CDK activity toward differentiation rather than division. We propose this cell cycle variant to exploit the existence of a cytoplasmic-or centriolar-CDK threshold lower than the S-phase threshold.

This shows that a cell can co-opt the cell cycle genetic program and regulate only certain elements to qualitatively and quantitatively divert CDK activity toward differentiation rather than division. We propose this cell cycle variant to exploit the existence of a cytoplasmic-or centriolar-CDK threshold lower than the S-phase threshold.

FBXO5 is a potential diagnostic and prognostic biomarker for HCC, and arbutin may exert anticancer effects through the suppression of FBXO5 expression.

This study determined that reduced EMI1 expression induces CIN and promotes cellular transformation, which is consistent with a role in early CRC development.