21May 2022
Altered splicing of ATG16‐L1 mediates acquired resistance to tyrosine kinase inhibitors of EGFR by blocking autophagy in non‐small cell lung cancer

Altered splicing of ATG16‐L1 mediates acquired resistance to tyrosine kinase inhibitors of EGFR by blocking autophagy in non‐small cell lung cancer

Resistance inevitably develops despite the initial efficacy of using tyrosine kinase inhibitors of epidermal growth factor receptors (EGFR‐TKIs) for treating patients with non‐small cell lung cancer (NSCLC). Recent studies highlight a link between alternative splicing and cancer drug response. Therefore, the study aimed to identify deregulated splicing events that play a role in resistance to EGFR‐TKI. The results support the role for defective autophagy in acquired resistance to EGFR‐TKIs and identify splicing regulation of ATG16‐L1 as a therapeutic vulnerability that could be explored for improving EGFR‐targeted cancer therapy.

  • #oncology

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