Beclin-1 Knockin Colon Cancer Cells
Genetically modified HCT116 colon cancer cells have been engineered to harbor specific D133A and D146A mutations in the Beclin-1 gene via AAV gene targeting. These cells, retaining a wildtype p53 status, exhibit a markedly slower growth rate while displaying an increased autophagic response. The genetic modification renders the Beclin-1 protein resistant to caspase-8 cleavage, thereby significantly altering the cellular response to anticancer agents. In vitro, these cells provide a robust model system to explore the intricate balance between autophagy and apoptosis, offering essential insights into cellular mechanisms governing drug resistance.
Description
This technology is differentiated by its novel approach to manipulating Beclin-1, as it represents the first model with cleavage-resistant mutations in this key regulatory protein. The unique genetic alterations facilitate more precise studies of the interplay between autophagy and apoptosis within a cancer context, enabling researchers to uncover new aspects of tumor progression and treatment resistance. Its creation through AAV gene targeting and subsequent comprehensive characterization underscores its potential as a powerful tool for advancing knowledge in cancer biology and drug discovery strategies.Applications
- Anticancer drug screening- Autophagy study platform
- Drug resistance evaluation
- Preclinical cancer model
Advantages
- Provides a unique platform for elucidating the interplay between autophagy and apoptosis in cancer cells.- Offers a novel tool to investigate mechanisms of resistance to anticancer agents.
- Enables testing of therapeutics targeting the autophagy pathway to improve cancer treatment strategies.
- Represents the first Beclin-1 knockin model, opening new avenues for research on Beclin-1’s role in cancer progression.