FBXW7 underexpression

FBXW7 overexpression promoted HOXA10 ubiquitination-based degradation and further inhibited BMP2 transcription, consequently restricting NPC cell proliferation in vitro and in vivo.

These effects were antagonized by FBXW7 downregulation or treatment with MHY1485. Our results suggest that FBXW7 improves cisplatin chemosensitivity and suppresses glycolysis in oSCC cells, indicating its promising potential as a target for puerarin to regulate the cisplatin sensitivity of oSCC cells.

FBXW7 inhibited tumorigenesis and apoptosis and enhanced radiosensitivity of NSCLC cells in vivo via the SOX9/CDKN1A axis. Overall, FBXW7 inhibited SOX9 expression by promoting SOX9 ubiquitination and proteasome degradation, suppressing the binding of SOX9 to CDKN1A, and upregulating CDKN1A, thereby improving the radiosensitivity of NSCLC cells.

This study demonstrates that MECP2 promotes the migration and invasion of GC cells by modulating the Notch1/c-Myc/mTOR signaling pathways via suppression of FBXW7 transcription. These findings suggest that MECP2 may be a novel effective therapeutic target in GC.

FBXW7 inhibited tumorigenesis and apoptosis and enhanced radiosensitivity of NSCLC cells in vivo via the SOX9/CDKN1A axis. Overall, FBXW7 inhibited SOX9 expression by promoting SOX9 ubiquitination and proteasome degradation, suppressing the binding of SOX9 to CDKN1A, and upregulating CDKN1A, thereby improving the radiosensitivity of NSCLC cells.

The combination of JQ1 with a Mcl-1 inhibitor (S63845) resensitized the FBW7 knockdown tumours to JQ1 treatment in vivo. Our study paves the way for a novel therapeutic potential of BETis with Mcl-1 inhibitors for BC patients with a low FBW7 expression.