FBXW7 overexpression

Furthermore, knockdown of FOXP4 led to decelerated growth of transplanted tumors and increased FBXW7 levels within the tumors. The findings of the current study underscore the regulatory role of FOXP4 in the transcription of FBXW7 and establish a clear link between aberrations in FBXW7 expression and the manifestation of malignant phenotypes in highly aggressive TC cells.

Our results suggest that FBXW7 affects autophagy through MCL1 in OSCC.

Sphere formation assay and qPCR showed FBXW7 was associated with ESCC stem cell formation. Our results suggest that FBXW7 may act as a tumor suppressor by repressing cancer stem cell formation and regulating tumor angiogenesis, cell senescence, DNA damage, and repair in ESCC.

In summary, these results unveiled that Fbxw7 targeted Nox1 for degradation, resulting in blocking the downstream Nox1-mTORC1 signaling to sensitize CRC cells to cisplatin. Our study potentiates that targeting the Fbxw7-Nox1-mTOR pathway could be an effective approach to overcome chemoresistance of colon cancer cells.

In conclusion, decreased expression of FBXW7 is confirmed in diverse OSCC cell lines. The enhanced FBXW7 expression inhibits cancer cell proliferation and promotes autophagy in both OSCC cells and xenograft tumor model.

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.

FBXW7 overexpression was herein shown to effectively sensitise OSCC cells to cisplatin treatment in vitro and in vivo.

In present study, we found that FBXW7 participates in the self-renewal, tumorigenicity, sorafenib therapy, and stem cell-like properties of HCC cells in vivo and in vitro...Furthermore, we found that ACTL6A overexpression inversed the self-renewal abilities and tumorigenic abilities depressed by overexpressing FBXW7. The current findings suggested that FBXW7 reduces the stemness of HCC cells by targeting and degrading ACTL6A and provides a novel target for the diagnosis and treatment of HCC.

Overexpression of SNHG4 and FBXW7 played an opposite role and abolished the effect of miR-25 overexpression. SNHG4 may interact with the miR-25/FBXW7 axis to suppress PTC cell proliferation.

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.

In addition, an interaction between FBXW7 and SREBP1a was confirmed by co-immunoprecipitation. Together, our data indicate that overexpression of FBXW7 prevents tumor growth of bladder cancer cells, likely through suppressing SREBP1a expression.

TUG1 knockdown promotes SIRT1-induced mitophagy by suppressing FBXW7-mediated SIRT1 degradation, thus relieving the neuronal apoptosis induced by CI/R injury. LncRNA TUG1 promotes neuronal apoptosis through inhibition of mitophagy. TUG1 decreased SIRT1 expression by promoting FBXW7-mediated SIRT1 ubiquitination. FBXW7/SIRT1 axis mediated the effect of TUG1 on OGD/R-induced neuronal apoptosis by regulating mitophagy.

In addition, miR-25 decreases the expression of FBXW7 protein to regulate autophagy. Therefore, miR-25 may represent a novel therapeutic target for the treatment of HCC.

Finally, FBXW7 and HDAC7 displayed an inverse correlation in glioblastoma tissues in vivo. Therefore, our data demonstrated an important function of FBXW7 in promoting glioblastoma apoptosis by interacting with HDAC7 and promoting HDAC7 ubiquitination.