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Gene network exploration of crosstalk between apoptosis and autophagy in chronic myelogenous leukemia
Fengfeng Wang1, William C S Cho2, Lawrence W C Chan1
1Department of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
Background:
Gene expression levels change to adapt the stress, such as starvation, toxin, and radiation. The changes are signals transmitted through molecular interactions, eventually leading to two cellular fates, apoptosis and autophagy. Due to genetic variations, the signals may not be effectively transmitted to modulate apoptotic and autophagic responses. Such aberrant modulation may lead to carcinogenesis and drug resistance. The balance between apoptosis and autophagy becomes very crucial in coping with the stress. Though there have been evidences illustrating the apoptosis-autophagy interplay, the underlying mechanism and the participation of the regulators including transcription factors (TFs) and microRNAs (miRNAs) remain unclear.
Results:
Gene network is a graphical illustration for exploring the functional linkages and the potential coordinate regulations of genes. Microarray dataset for the study of chronic myeloid leukemia was obtained from Gene Expression Omnibus. The expression profiles of those genes related to apoptosis and autophagy, including MCL1, BCL2, ATG, beclin-1, BAX, BAK, E2F, cMYC, PI3K, AKT, BAD, and LC3, were extracted from the dataset to construct the gene networks.
Conclusion:
The network analysis of these genes explored the underlying mechanisms and the roles of TFs and miRNAs for the crosstalk between apoptosis and autophagy.
Insights
Gene expression changes during stress impact apoptosis and autophagy. Network analysis reveals how transcription factors and microRNAs regulate this crucial cellular balance, offering insights into disease.
Area of Science:
- Molecular Biology
- Genetics
- Cellular Biology
Background:
- Cellular stress responses, including starvation and radiation, alter gene expression.
- These alterations modulate apoptosis and autophagy, critical cellular fates.
- Genetic variations can disrupt these responses, potentially leading to cancer and drug resistance.
Purpose of the Study:
- To investigate the interplay between apoptosis and autophagy.
- To elucidate the mechanisms and regulatory roles of transcription factors (TFs) and microRNAs (miRNAs) in this crosstalk.
Main Methods:
- Utilized a gene network approach to visualize gene interactions.
- Extracted gene expression profiles related to apoptosis and autophagy from a chronic myeloid leukemia microarray dataset.
- Constructed gene networks using key genes such as MCL1, BCL2, ATG, beclin-1, BAX, BAK, E2F, cMYC, PI3K, AKT, BAD, and LC3.
Main Results:
- Gene network analysis provided a graphical representation of functional linkages.
- Identified potential coordinate regulations among genes involved in apoptosis and autophagy.
- Visualized the complex interactions within the apoptosis-autophagy pathway.
Conclusions:
- Network analysis successfully explored underlying mechanisms of apoptosis-autophagy crosstalk.
- Highlighted the significant roles of transcription factors and microRNAs in regulating this cellular process.
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