Publications by authors named "Nai Yang Yeat"
Article Synopsis
- Aberrant activation of EGFR contributes to the growth of non-small cell lung cancer (NSCLC) and resistance to treatment with EGFR tyrosine kinase inhibitors (TKIs), largely due to mutations and c-MET amplification.
- The study identifies WDR4 as a key protein that, when overexpressed, leads to the degradation of PTPN23, which is important for lysosome function and the turnover of EGFR and c-MET, ultimately aiding cancer cell proliferation and metastasis.
- Targeting the WDR4-PTPN23 interaction offers a promising strategy to enhance EGFR and c-MET degradation, potentially improving treatment outcomes for patients with EGFR TKI-resistant NSCLC.
Activation of tumor-intrinsic innate immunity has been a major strategy for improving immunotherapy. Previously, we reported an autophagy-promoting function of the deubiquitinating enzyme TRABID. Here, we identify a critical role of TRABID in suppressing anti-tumor immunity.
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