An autophagy-inducing stapled peptide promotes c-MET degradation and overrides adaptive resistance to sorafenib in c-MET⁺ hepatocellular carcinoma.

ABSTRACT:

Background

Hepatocellular carcinoma (HCC) accounts for approximately 90% of primary liver cancer cases and ranks as the second leading cause of cancer related death. Multiple receptor tyrosine kinases such as EGFR, FGFR and c-MET have been shown to drive tumorigenesis and progression of HCC. However, tyrosine kinase inhibitors (TKIs) that target these kinases, including the FDA-approved sorafenib, only offer limited clinical success. Resistance to sorafenib and other TKIs also readily emerge in HCC patients, further limiting the usage of these drugs. Novel therapeutic strategies are needed to address the urgent unmet medical need for HCC patients.

Results

Autophagy is an evolutionally conserved lysosome-dependent degradation process that is also functionally implicated in HC

SUBMITTER: Gao S 

PROVIDER: S-EPMC9791588 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature