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Chelerythrine inhibits esophageal squamous cell carcinoma progression via PINK1-Parkin-mediated mitophagy
Chelerythrine may slow esophageal cancer growth by boosting cell cleanup through the PINK1-Parkin pathway
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Abstract
Chelerythrine (CHE) significantly reduced tumor size and weight in nude mice bearing KYSE150 tumors.
- CHE inhibited the proliferation, migration, and invasion of esophageal squamous cell carcinoma (ESCC) cells in a dose-dependent manner.
- The compound induced cell apoptosis and triggered cell death through a specific pathway involving PINK1 and Parkin, linked to increased reactive oxygen species in mitochondria.
- CHE altered the production of autophagosomes and autolysosomes when used with autophagy inhibitors, indicating its role in complete autophagic flux.
- The treatment affected various signaling pathways related to protein degradation, , and mitochondrial energy metabolism.
- CHE also reduced the presence of M2 macrophages in the tumor microenvironment and influenced cell metabolism.
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Key numbers
> 90%
Inhibition Rate
Percentage inhibition of cell viability at 30 µM concentration.
5.616 µM, 10.80 µM, 10.76 µM
Values
Half maximal inhibitory concentration for KYSE30, KYSE150, and KYSE450 cells, respectively.
Significantly decreased
Tumor Weight Reduction
Tumor weight in -treated mice vs. control group.