2023 World Conference on Lung Cancer (Posters)-P1.08. Exploring Autophagy Flux-Related Molecules for Overcoming EGFR TKI Resistance

P1.08. Exploring Autophagy Flux-Related Molecules for Overcoming EGFR TKI Resistance - PDF(Slides)

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The study aimed to identify autophagy flux-related molecules associated with acquired resistance in mutant EGFR non-small cell lung cancer. The researchers established resistant cell lines through prolonged exposure to Osimertinib and Erlotinib. They analyzed the protein expressions of autophagy flux molecules and explored genes that induce autophagy flux activity. They also evaluated the protein expression of autophagy flux-related molecules using immunohistochemistry in tissue microarrays.<br /><br />In vitro studies showed that autolysosomes were accumulated in the resistant cell lines, along with increased protein expression of LC3B and p62. Through mRNA sequencing and qRT-PCR, the researchers identified autophagy flux-related molecules that were significantly increased in the resistant cells. In clinical studies, they found that the expression of certain autophagy flux-related molecules was significantly higher in mutant EGFR NSCLC compared to wild-type NSCLC. They also observed differences in expression based on different EGFR mutation subtypes.<br /><br />The findings indicate that autophagy flux-related signaling molecules and known genetic variants are strongly associated with resistance acquired during EGFR TKI treatment in mutant EGFR NSCLC patients. The researchers conclude that further functional studies are needed to explore the potential of these autophagy-related genes as targets for overcoming EGFR TKI resistance.<br /><br />This research was supported by the Basic Science Research Program through the National Research Foundation of Korea.

Asset Subtitle

Jin-Hyoung Kang

Meta Tag

Speaker Jin-Hyoung Kang

Topic Tumor Biology: Translational Biology - Drug Resistance

Keywords

autophagy flux

acquired resistance

mutant EGFR

non-small cell lung cancer

Osimertinib

Erlotinib

protein expressions

immunohistochemistry

EGFR mutation subtypes

EGFR TKI resistance