2023 World Conference on Lung Cancer (Posters)-EP02.01. CSNK1D and CSNK1E Inhibition Regulates Autophagy by Promoting Autophagic Flux in Lung Cancer

EP02.01. CSNK1D and CSNK1E Inhibition Regulates Autophagy by Promoting Autophagic Flux in Lung Cancer - PDF(Abstract)

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This study investigates the role of Casein Kinase I family members CSNK1D and CSNK1E in modulating autophagy in lung cancer cells. Autophagy is a cellular process involved in maintaining cell homeostasis, and dysregulation of autophagy has been implicated in tumorigenesis. The researchers constructed plasmids to inhibit the expression of CSNK1D and CSNK1E in 293T cells and observed the effects on autophagy-related genes SQSTM1/p62 and LC3. They found that inhibiting CSNK1D and CSNK1E led to a decrease in SQSTM1/p62 protein levels and an increase in the LC3II/I ratio, indicating increased autophagy. Using transmission electron microscopy, they observed an increase in the number of autophagosomes and autophagic lysosomes in lung cancer cells (A549) after inhibiting CSNK1D and CSNK1E. Additionally, the researchers treated the cells with a lysosomal inhibitor and found that CSNK1D/E inhibition resulted in the accumulation of LC3 protein, further supporting the induction of autophagy. Using a reporter system, they detected an increase in autophagic flux in A549 cells with CSNK1D and CSNK1E knockdown. Overall, the study provides evidence for the role of CSNK1D and CSNK1E in autophagy regulation and suggests their potential as therapeutic targets in lung cancer. The research was supported by the National Natural Science Foundation of China, and the authors acknowledge the assistance of the Instrument Analysis Center of Shenzhen University.

Asset Subtitle

Vivian Weiwen Xue

Meta Tag

Speaker Vivian Weiwen Xue

Topic Tumor Biology: Preclinical Biology - Molecular Therapeutic Targets

Keywords

CSNK1D

CSNK1E

autophagy

lung cancer cells

SQSTM1/p62

LC3

transmission electron microscopy

lysosomal inhibitor

autophagic flux

therapeutic targets