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Updated: Feb 4, 2026

Author Spotlight: Understanding Cytokine-Induced Cell Death in Intestinal Epithelial Cells Using Human Organoids
Published on: August 2, 2024
Protein kinase C Inhibitors selectively modulate dynamics of cell adhesion molecules and cell death in human colon
Muzaffer Dükel1,2, Zehra Tavsan2, Duygu Erdogan3
1a Moleculer Biology and Genetic Department, Faculty of Art and Science , Mehmet Akif Ersoy University , Burdur , Turkey.
Abstract:
During development of colon cancer, Protein Kinase Cs (PKCs) are involved in regulation of many genes controlling several cellular mechanisms. Here, we examined the changes in cell adhesion molecules and PKCs for colorectal cancer progression. We identified that PKCs affected expression of EpCAM, claudins, tetraspanins. Treatment with low concentrations of PKC inhibitors resulted in decreased cell viability. In addition, immunoblotting and qRT-PCR analysis showed that apoptosis was inhibited while autophagy was induced by PKC inhibition in colon cancer cells. Furthermore, we observed decreased levels of intracellular Reactive Oxygen Species (ROS), lipid peroxidation and protein carbonyl, confirming the ROS-induced apoptosis. Taken together, our results reveal that PKC signalling modulates not only cell adhesion dynamics but also cell death-related mechanisms. Abbreviations: PKC: Protein Kinase C; EpCAM: Epithelial cell adhesion molecule; FBS: fetal bovine serum; MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide); CAM: cell adhesion molecule; ROS: reactive oxygen species.
Insights
Protein Kinase Cs (PKCs) influence colorectal cancer progression by altering cell adhesion and death pathways. Inhibiting PKCs reduces cancer cell viability and triggers autophagy, offering potential therapeutic strategies.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Protein Kinase Cs (PKCs) play a role in regulating genes involved in cellular mechanisms during colon cancer development.
- Understanding the role of PKCs in cell adhesion and death pathways is crucial for advancing colorectal cancer therapies.
Purpose of the Study:
- To investigate the impact of Protein Kinase Cs (PKCs) on cell adhesion molecules and their role in colorectal cancer progression.
- To explore the effects of PKC inhibition on colon cancer cell viability, apoptosis, and autophagy.
Main Methods:
- Analysis of cell adhesion molecules (EpCAM, claudins, tetraspanins) and PKC expression.
- Treatment of colon cancer cells with PKC inhibitors at low concentrations.
- Assessment of cell viability using MTT assay.
- Immunoblotting and qRT-PCR to evaluate apoptosis and autophagy.
- Measurement of intracellular Reactive Oxygen Species (ROS), lipid peroxidation, and protein carbonyl levels.
Main Results:
- PKC signaling was found to affect the expression of EpCAM, claudins, and tetraspanins.
- Low concentrations of PKC inhibitors decreased colon cancer cell viability.
- PKC inhibition led to suppressed apoptosis and induced autophagy in colon cancer cells.
- Reduced intracellular ROS, lipid peroxidation, and protein carbonyl levels were observed, supporting the inhibition of ROS-induced apoptosis.
Conclusions:
- PKC signaling is a key regulator of cell adhesion dynamics in colorectal cancer.
- PKC inhibition modulates cell death mechanisms, including apoptosis and autophagy.
- These findings highlight the potential of targeting PKC signaling for colorectal cancer treatment.
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