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AMPK activation reduces cancer cell aggressiveness via inhibition of monoamine oxidase A (MAO-A) expression/activity
Chandreyee Datta1, Payel Das1, Subhajit Dutta1
1Department of Biotechnology, National Institute of Technology, Durgapur, Mahatma Gandhi Avenue, 713209 Burdwan, West Bengal, India.
Aim:
AMPK can be considered as an important target molecule for cancer for its unique ability to directly recognize cellular energy status. The main aim of this study is to explore the role of different AMPK activators in managing cancer cell aggressiveness and to understand the mechanistic details behind the process.
Main Methods:
First, we explored the AMPK expression pattern and its significance in different subtypes of lung cancer by accessing the TCGA data sets for LUNG, LUAD and LUSC patients and then established the correlation between AMPK expression pattern and overall survival of lung cancer patients using Kaplan-Meire plot. We further carried out several cell-based assays by employing different wet lab techniques including RT-PCR, Western Blot, proliferation, migration and invasion assays to fulfil the aim of the study.
Key Findings:
SIGNIFICANCE: This study identifies the importance of AMPK activators as a repurposing agent for combating lung and colon cancer cell aggressiveness. It also suggests SRT-1720 as a potent repurposing agent for cancer treatment especially in NSCLC patients where a point mutation is present in LKB1.
Insights
AMPK activators can combat cancer cell aggressiveness. SRT-1720 is a promising repurposed drug for lung cancer, particularly non-small cell lung cancer (NSCLC) with LKB1 mutations.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- AMP-activated protein kinase (AMPK) is a key regulator of cellular energy homeostasis.
- AMPK plays a crucial role in cancer development and progression.
- Understanding AMPK's role is vital for developing novel cancer therapies.
Purpose of the Study:
- To investigate the role of AMPK activators in modulating cancer cell aggressiveness.
- To elucidate the underlying mechanistic details of AMPK's action in cancer.
- To identify potential therapeutic agents for cancer treatment.
Main Methods:
- Analyzed AMPK expression patterns in lung cancer subtypes using TCGA data.
- Correlated AMPK expression with overall survival via Kaplan-Meier plots.
- Performed cell-based assays (RT-PCR, Western Blot, proliferation, migration, invasion) to assess AMPK activator effects.
Main Results:
- Identified AMPK activators as potential repurposing agents for lung and colon cancer.
- SRT-1720 demonstrated significant efficacy in combating cancer cell aggressiveness.
- Highlighted SRT-1720's potential in treating NSCLC patients with LKB1 mutations.
Conclusions:
- AMPK activators hold promise for repurposing in cancer therapy.
- SRT-1720 is a potent candidate for repurposing, especially in specific NSCLC contexts.
- Further research into AMPK-targeted therapies could lead to improved cancer management strategies.
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