WEE1 stabilizza MYC per promuovere la resistenza terapeutica nel carcinoma epiteliale dell'esofago.

Esophageal adenocarcinoma (EAC) is an aggressive malignancy with poor patient outcomes and limited therapeutic options. WEE1, a G2/M checkpoint kinase, is often upregulated in cancers and associated with resistance to therapy. In this study, we identify a previously unrecognized cytoplasmic role of WEE1 in stabilizing the oncogenic transcription factor MYC and promoting drug resistance in EAC. WEE1 was found to be aberrantly overexpressed and mislocalized to the cytoplasm in EAC cell lines and patient samples. WEE1 depletion or inhibition by MK-1775 significantly reduced MYC protein levels and transcriptional activity by promoting proteasome-mediated degradation. Mechanistically, WEE1 inhibi